NEURODIAGNOSTIC POLICIES & PROCEDURES MANUAL

Stanford University Hospital Department of Neurology Quality Assurance Plan

Reviewed and revised 26 July 2010

STANFORD NEURODIAGNOSTIC LABORATORY QUALITY ASSURANCE PROCEDURE

Step I:

Responsibility

The Director of the Neurodiagnostic Laboratory is responsible for directing the quality assurance program on a continuous basis. Responsibilities are delegated by this individual to various members of the service/department and hospital personnel. A. Neurodiagnostic Laboratory Quality Assurance Committee 1. 2. 3. 4. 5. 6. 7. Reviews and approves the Medical Service Quality Assurance plan. Identifies important aspects of care. Identifies the aspects of care to be monitored and establishes thresholds for unwanted results. Oversees the monitoring and evaluation process for selected aspects of medical care. Tracks identified problems to their resolution. Evaluates effectiveness of quality assurance activities. Reports periodically to the Executive Quality of Care Committee.

B. Manager, Neurodiagnostic Laboratory 1. 2. 3. 4. Implements the EEG laboratory Quality Assurance Program. Develops plans and takes action to resolve. Evaluates the effectiveness of actions taken. Orients and educates staff regarding the EEG Laboratory Quality Assurance Program.

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Step III: Important Aspects of Care Three factors are considered in selecting the aspects of care that are important for monitoring quality and appropriateness of care. One or more of the following descriptors will result in monitoring. A particular aspect of care that A. High Volume occurs frequently or affects large numbers of patients. B. High Risk Patients are at risk for serious consequences or are deprived of substantial benefit if the aspect of care is not provided correctly, in a timely manner, or based upon proper indication. An aspect of care which historically has produced problems for staff or patients.

C.

Problem Prone

The Neurodiagnostic Laboratory has identified the following aspects of care. A. B. C. D. Technical quality Professional interpretation Appropriateness of study Timeliness of service

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Step IV: Indicators & Step V: Establish Threshold Indicators call attention to areas of care that need to be evaluated further. These indicators will also serve as a data collection method for the important aspects of care. In addition to hospital-wide and generic indicators, the Neurodiagnostic Laboratory has chosen the following possible indicators for the Neurodiagnostic Laboratory. A. Technical quality 1. 2. Technologist interpretation sheet Ongoing technologist training a. b. c. attend at least 5 reading sessions/month* attend at least 1 conferences/ month* attend at least 4 monthly staff meetings/year* Threshold >95% >98%

* when not on vacation or other leave B. Professional interpretation 1. All procedures will be interpreted by board >100% certified or board eligible faculty All neurophysiologists will review 10 procedures yearly interpreted by other electroencephalographers to ensure accuracy of interpretation >80%

2.

C. Appropriateness of study 1. D. 5% of all procedures will be reviewed quarterly for appropriateness >75%

Timeliness of service 1. Data acquisition-5% of all procedures will >90% be reviewed quarterly

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D.

Timeliness of service (Cont) a. b. c. inpatient procedures will be done within 24 hours of receiving order outpatient procedures will be scheduled within 7 days of order, unless otherwise requested Emergency procedures will be done immediately or within 2 hours

Threshold

2.

5% of reports will be reviewed quarterly for timeliness a. The hard copy will be available within 1 working day of the time the procedure is done or on the Monday following a weekend study

>95%

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Step VI: Collect and Analyze Data Data collection methods will reflect the type of indicator. The two most common methods of data collection are reviewing the pertinent documentation, and observation of the patient or health care provider. Many documents and activities are potential data sources for quality assurance purposes. They include, but are not limited to the following: Physician activity reports - Care review committee reports (incident reports) - Neurodiagnostic data base Data can be collected prospectively, concurrently or retrospectively. Prospective - data collection occurs prior to the delivery of care Concurrent - data collection occurs simultaneously with the delivery of care Retrospective- data collection occurs following the delivery of care or after discharge Concurrent data collection is preferred. This facilitates access to data sources, and concurrent review creates an opportunity to correct a potential problem or enhance the quality of care provided.

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Step VII: Evaluate Based Upon Thresholds After data collection and tabulation, the findings will be analyzed and evaluated based on established threshold levels. When an indicator exceeds the threshold level, the data and/or event, clusters of similar events, care provided by an individual, a group of providers on a particular unit or shift, or any relevant subset. The evaluation is aimed at discovering the factors contributing to sub-optimal care so an appropriate corrective action can be developed. In addition, individual case reviews and cumulative data are evaluated at the EEG Laboratory. The evaluation will consider the quality and appropriateness of care for individual and aggregate data. The Neurodiagnostic Laboratory committees to request periodic quality of care information: Medical records Care review will contact the following forwarding of relevant

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Step VIII: Take Action Generally, a specific action plan will be implemented only when the unwanted results are greater than the pre-determined threshold. Plans will be developed to address the source of the problem. The remedy should enhance the quality of care. Problems or sub-optimal care are commonly caused by three factors: defects in systems lack of knowledge problems in performance A written plan for response will accompany the summary report of the data and will be submitted periodically. The plan will address the following points: who is responsible for implementing the actions - who or what is expected to change - what action will be taken (that is appropriate in view of the cause, scope, and severity of the problem) - when is the change expected to occur

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Step IX: Assess Effectiveness of Actions Whenever actions are taken, they will be evaluated for efficacy and documented for future reference. Actions will be carefully evaluated for both a positive and a negative impact. Plans and their results will be recorded in Quality Assurance Reports. In addition, the plans and results may appear in the minutes of Department Meetings and Quality Assurance Committee Meetings. Quality Assurance activities within the hospital will be evaluated annually by the Executive Quality of Care Committee.

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Step X:

Communicate Results

Regular reports of the Neurodiagnostic Laboratory quality assurance activities will be made to the Deputy Chief of Staff's office. Reports of the overall quality assurance issues, evaluations, actions and results are submitted annually to the Executive Quality of Care Committee, as well as the Deputy Chief of Staff's office. Individual physicians will receive a profile of their activity on an annual or more frequent basis. Reports of the Neurodiagnostic Laboratory Quality Assurance findings will be communicated to appropriate Clinical Services and Hospital Departments: Neurology Neurosurgery Medicine Nursing Medical Records

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STANFORD UNIVERSITY MEDICAL CENTER

DEPARTMENT OF NEUROLOGY AND NEUROLOGICAL SCIENCES STANFORD, CALIFORNIA CALIFORNIA 94305-5235 FAX (415) 725-7459

STANFORD COMPREHENSIVE EPILEPSY CENTER ADMISSION DIAGNOSIS PROTOCOLS FOR PATIENTS ADMITTED TO E-GROUND EPILEPSY MONITORING UNIT (EMU) I. Purpose: To identify patients being admitted to the Epilepsy Monitoring Unit. Patients admitted for continuous video EEG monitoring fall into one of four diagnostic categories: A. Differential diagnosis

Patients admitted for differential diagnosis will have continuous video EEG monitoring in order to characterize their clinical events (i.e. are these epileptic seizures?). Usually several of their typical events will be recorded. During this hospitalization the patient may require a psychiatric or psychological evaluation. Depending on the individual case, a neuropsychological evaluation may be necessary as well. Once several of the events have been recorded, the patient will be discharged with instructions for antiepilepsy therapy, ongoing psychological care or will be released to their referring physician. B. Seizure classification

The purpose of this admission to the EMU is to determine the exact seizure type by EEG so that proper therapy can be either initiated or continued. During this hospitalization a psychiatric or psychological evaluation may be necessary. Upon discharge the patient will be started or continued on the appropriate antiepilepsy medicine. If the patient has been treated with the appropriate medicine and continues to have seizures, the patient may go on to a surgical evaluation or may be a candidate for one of the investigational antiepilepsy drugs. C. Quantification of seizure frequency

These patients are admitted for continuous video EEG monitoring in order to precisely determine the seizure frequency. There may be a concern that not all the patients' events are seizures. Alternatively, patients may not know when they are

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Protocol Cont'd. having seizures and may underestimate the frequency. A psychiatric/psychological evaluation may be required. Upon discharge these patients will be maintained on antiepilepsy medicine, may need psychological follow-up and may require further evaluation for surgery or investigational antiepilepsy drugs. D. Surgical evaluation Patients are admitted for continuous video EEG monitoring to determine the exact location of onset of their seizures. During Phase I of the evaluation, several seizures will be recorded with scalp and occasionally with special electrodes, such as sphenoidal electrodes. Neuropsychological testing will be performed and in some cases a psychiatric consult may be obtained. Prior to this hospitalization patients will have an MRI of the brain and routine EEG's. Before discharge from the hospital patients may be scheduled for a SPECT and/or a PET scan. During phase II of the surgical evaluation, patients will be re-admitted to the hospital for implantation of intracranial electrodes. Once the electrodes have been implanted, seizures are recorded by continuous video EEG monitoring. If needed, during this phase of evaluation a psychiatric consult will be obtained. If patients are candidates for surgery, they will then enter phase III of the surgical evaluation. They will be admitted to the hospital for a Wada test (or the test can be done as a monitored outpatient)and temporal lobectomy or other resection. Patients will be released home on antiepilepsy medicine.

Approved by: Robert S. Fisher, MD, PhD Original date: 1/91, updated 7/26/2010 MM/ag

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Background Information The kind of radioactive material used is "Technetium 99m", the element's name is technetium, and the number describes the nuclear weight, which is the number of neutrons + protons in the nucleus. Technetium-99m is abbreviated as "Tc-99m, 99m, or Tc 99mThe Tc 99m is attached to a pharmaceutical that allows the material to be localized in a specific tissue so that an image can be made.
.

Tc 99m has a half life of about 6 hours. This means that one-half of the radioactive atoms undergo a change in 6 hours. Half of those remaining undergo a change in the next 6 hours, and so on. In 24 hours the initial activity decays to 1/16 of the original, in 42 hours 1/128, etc.
-

When an atom of Tc99 undergoes a change it gives of a gamma ray. A gamma ray is very similar to an X-ray. The energy of Tc 9 m gamma rays is has very similar to diagnostic X-rays. It is relatively easy to shield Tc99m gamma rays using lead -- 1/100th of an inch of lead reduces the amount of gamma radiation from Tc 99m by one half. A second layer reduces it by half again and so on. Syringes are equipped with lead shielding to significantly reduce the dose to the person making the injection. (Do not remove the syringe from its protective shield. Do not recap the syringe.) Radiation exposures are measured in units called milliroentgens which are approximately equivalent to another unit of radiation dose called millirems (abbreviated as mrem). Frequently we talk about the dose rate. That is the amount of radiation dose per hour, i.e., millirem/hr. Workers are permitted to get doses up to 5000 millirems in a year. At Stanford we try to limit doses to less than 10 percent of the limits, i.e., less than 500 millirems per year. Limits to the hands and feet, skin only, and to the lens of the eye are higher. The doses to the public are more limited -- 100 millirems per year. This is almost the same as the amount of radiation that we receive from background. The amount of radioactivity is measured in units called millicuries (abbreviated as mCi), this indicates the number of atoms that are undergoing changes each second. The amount of radioactivity, i.e.,

of Tc 99m , given to a patient for this procedure is usually about 20 millicuries. The dose rate from the gamma rays at 1 foot from 1 millicurie of Tc 99'n without any shielding is about 0.7 millirem per hour. (If one's finger is 1 centimeter from an 1 millicurie source of TO', unshielded, the dose rate is about 700 millirem/hour. See inverse square law, below.) Radiation occurs naturally. We all are exposed all of the time to radiation that comes from radioactive elements in our bodies and in materials around us, we also receive radiation from the sun and stars The total amount of radiation received annually by persons in this area (San Francisco Bay area) is about 100 millirem. If one moves to places where rocks contain more radioactive elements (such as places with granite rocks) or move up in elevation or towards the earth's poles the radiation doses increase. For example, the radiation dose to persons living in Denver, Colorado is about twice that which we receive (about 180 millirem, annually.) The principal concerns about possible health effects from radiation are the possible increase in cancer, mutations in germ cells, and effects on the fetus (primarily the risk of childhood cancer in those exposed.) The risks associated with radiation doses are among the most thoroughly studied of all cancer causing and mutagenic agents. The risks at very low doses -such as those which Stanford workers receive -- are estimated from those who have received very high doses compared to occupational dose limits. It is probable, therefore, that the estimate is conservative. The risk of causing fatal cancer that is associated with a single dose of 10,000 millirem was estimated in 1990 by a committee of the National Academy of Sciences to be about 500 in 100,000 for persons of working age. The normal risk of fatal cancer in that group is about 1 in 5 to 1 in 6 (gender dependent). Thus, the added risk of that dose (10,000 millirems) is about 1/40 of the normal risk. The genetic risk from a dose of 1000 millirems to the gonads of either parent is about I in 10,000. The normal incidence of genetic defects in live births is about 6/100. The added risk of a dose of 1000 millirems is about 1/600 of the normal risk. The added risk of fatal childhood cancer in those who receive a dose of 1000 millirems in utero is about 1 in 1000. This is still a small added risk, but is the largest comparative risk; therefore, regulations allow for a woman who declares in writing to the Radiation Safety Officer that she is

pregnant, to require management to restrict the dose of radiation to her conceptus to 500 millirems for the full term of the pregnancy, and to limit the dose to less than 50 millirem in any month. (Given that fact that the _ Stanford guideline is 500 millirems to workers, it is unlikely that the fetus would receive such a dose in any case.) Protection against external radiation (radioactivity in the syringe or in the patient) is accomplished by applying three basic principles: Shielding, as described above. The radioactivity is contained in a shielded syringe. Time -- Since a dose is produced at a rate (e.g., millirems/hour), the less time one is exposed to the source. The less the total dose and the less the consequent risk will be. Generally plan ones activities to minimize time of exposure. Distance - the dose from a source drops rapidly as one moves away from the source. Double the distance -- one fourth of the dose. Three times the distance -- one ninth of the dose. Ten times the distance -- 1/100 of the dose... This is called the inverse square law of radiation.

It is important to keep radioactivity out of one's body, since the radioactive atoms would be in contact with cells and tissues and would give a radiation dose to them. To protect against getting radioactivity into one's body, one practices "Universal Precautions". Wear latex gloves, a lab coat, smock or gown, and protective eye gear. Wash hands thoroughly after handling the syringe. Also, do not recap the syringe after use. Contamination from the radioactivity can also gain access to one's body. Clean up spills promptly. Report spills immediately to Health Physics.

RADIATION PROTECTION WEAR LAB COAT (GOWN OR SMOCK) AND DISPOSABLE LATEX GLOVES WHEN HANDLING RADIOACTIVE MATERIALS WASH HANDS THOROUGHLY AFTER HANDLING RADIOACTIVITY. COVER WORKING SURFACES WITH ABSORBENT PAPER THAT HAS NONPERMEABLE PLASTIC COATING ON THE BACK SIDE. INCONTINENCE PADS ARE A GOOD TYPE OF PROTECTIVE COVERING. CLEAN UP SPILLS IMMEDIATELY. PUT WASTE IN A PLASTIC BAG (WEAR GLOVES AND LAB COAT). DO NOT WALK IN SPILL. OPERATING ROOM TYPE OF SHOE COVERS WILL PROTECT SHOES. (ALWAYS CALL HEALTH PHYSICS, IF SYRINGE IS SPILLED.) DO NOT EAT, OR DRINK IN THE AREA WHEN HANDLING RADIOACTIVE MATERIALS. WEAR ASSIGNED FILM BADGE WHEN HANDLING RADIOACTIVE DOSE. DO NOT STORE THE BADGE NEXT TO THE RADIOACTIVITY. NOTIFY HEALTH PHYSICS IN THE EVENT OF SPILL OR OTHER EMERGENCY -- 723-3201 (24 HOURS.)

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS

TABLE OF CONTENTS 1. 2. Scope of Service EEG Lab Policies & Procedures 2.1 General Polices 2.2 Routine EEG Protocol 2.3 Guidelines for Routine Activations 2.4 Standard EEG Montages 2.5 ECS Protocol Epilepsy Monitoring Testing Policies 3.1 General Policies 3.2 Protocol for Phase I Patients 3.3 Protocol for Phase II Patients Intraoperative Monitoring Policies 4.1 General Policies 4.2 Electrode Setups and Montages Wada Testing Protocol Botulinum Toxin Policy and Procedure Neuropsychology Service Policy and Procedure Sedation Policies 8.1 General Policies 8.2 Drug Information Sheets 8.3 Conscious Sedation Protocols Testing Instructions for Patients 9.1 EEG Instructions 9.2 EMG Instructions 9.3 Ambulatory EEG Instructions

3.

4.

5. 6. 7. 8.

9.

10.

Infection Prevention Policies 10.1 EEG Procedures 10.2 EMG Procedures 10.3 Intraoperative Monitoring Procedures

11. Age Specific Competency Assessment for END Techs 12. Overtime Policy 1 3 . Consent to Photograph 1 4 . EH&S Air Monitoring Report for Ethyl Ether.

STANFORD HOSPITAL AND CLINICS DEPARTMENT PLAN FOR PROVIDING SERVICE Department/Unit: NEURODIAGNOSTIC LABS

I.

Scope of Service
The Neurodiagnostic Labs provides neurological testing procedures to all ages from neonates to geriatrics. Services are provided to both in and out patient populations with suspected or known neurological dysfunctions and disorders. Testing and treatment procedures provided by the Neurodiagnostic labs include: EEGs, EMGs, Nerve Conduction Studies, Evoked Potentials, Long Term Epilepsy Monitoring, Infra-operative Neurophysiologic Monitoring, Neuropsychological Testing, Movement Disorder Analysis, Trancranial Dopplers, and Botulinum Toxin Injections. Monday Friday, 7:30 am to 4:30 pm. On-call service provided for EEG, Epilepsy Monitoring, IOM, and TCD procedures outside of regular staffing hours, including evenings, weekends and holidays.

II.

Criteria for Entry/Admission to Service (Patient Care Departments only)

Any patients with suspected or known neurological dysfunction are appropriate for testing or treatment in the Neurodiagnostic labs. Also patients who are at risk of suffering loss of neurological function during surgical procedures are monitored through lab services.

III.

Staffing
Staffing levels are based on patient testing volume. The mix of staff includes technologists (EEG and EMG), licensed professionals (Neuropsychologists), Neurologists and administrative personnel. Technologists perform all noninvasive testing procedures. Physicians perform all invasive procedures (e.g. EMG, Botulinum Toxin Injections). Physician staff interprets all test procedures. The technical staff is cross-trained to allow the ability to adjust appropriate level of staffing due to workload demands in each area of service.

IV. Qualifications of Staff

Technologists must meet the qualifications and competencies set by the American Society of Electroneurodiagnostic Technologists. All techs are registered or endeavor to become registered by the American Board of Registered Electroneurodiagnostic Technologists. Technical staff attends weekly conferences, and grand rounds in Neurology and Neurosurgery and the yearly Clinical Update in Neuroscience Symposium. Efforts are made to allow technologists to attend conferences and workshops outside of the institution in order to maintain their continuing education

Department Plan for Providing Service

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V.

Description of Communication/Collaboration and Functional Relationships with Other Departments and Services
The Neurodiagnostic labs work closely with the departments of Neurosurgery, Interventional Neuroradiology, ENT and Orthopedic surgery in providing Infra-operative monitoring services. The Neuropsychology service interfaces with the Department of Psychiatry to provide evaluations on specified in-patients.

VI. Goals of Department/Service

1. Provide excellent quality service in all areas of neurodiagnostic testing. 2. Strive to increase volume in all service areas of the labs 3. Operate efficiently and effectively in providing services.

VII. Plan to Improve Quality of Service

1. Develop patient feedback system to improve quality of service. 2. Perform improvements to physical lab space to provide better testing environment. 3. Improve continuing education of technologists to maintain their level of competency in changing areas of neurological testing.

VIII. Additional Standards of Practice Adopted/Adapted by Department/Service (Patient Care Departments only)
Procedures are performed to follow guidelines of the American Society of Clinical Neurophysiology, the American Association of Electrodiagnostic Medicine, the American Board of Psychiatry and Neurology, the American Board of Professional Neuropsychology and the American Board of Clinical Neuropsychology.

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS STANFORD UNIVERSITY HOSPITAL EEG LABORATORY General Policies 1. The EEG laboratory will perform EEGs to meet the "Minimum Technical Requirements for Performing Clinical Electroencephalography" and the "Standards for Practice Guidelines in Clinical Electroencephalography" set forth by the American EEG society. ( Journal of Clinical Neurophysiology 11(1):2-5, 14-15, Raven Press, 1994)Location: Stanford Hospital , CORE building, ROOM #H3132 2. Hours of operation: Monday to Friday, 08:00 to 17:00 hours The EEG Lab is covered on an on-call basis 24 hours a day and on weekends. A monthly on-call schedule is provided to the hospital paging operator detailing the technologist on evening and weekend call. For EEGs requested on-call the study must be approved by the attending neurologist or the electroencephalographer oncall before it can be performed.

3. The EEG Laboratory will perform electroencephalograms on patients referred by licensed physicians. Physicians can be members of the medical staff of Stanford University Hospital or licensed physicians in the state of California. An EEG request form should be completely filled out for each outpatient. Inpatients will be ordered through the hospital SMIS system. 4. The EEG Laboratory shall provide physicians with accurate reports on EEGs performed in the laboratory within 24 hours of the recording. 5. Instructions will be given to patients concerning their EEG either through the printed EEG Instruction sheet or by phone.

Rev 3/98

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS

STANFORD UNIVERSITY HOSPITAL EEG LABORATORY II. Routine EEG Protocol The following protocol applies to routine EEG recordings: Awake, Sleep, Awake/Sleep with TI & T2, and non-ECS portable recordings. Efforts should be made to do all recordings on digital EEG equipment (Nicolet Voyageurs) whenever possible. Portable recordings will be done on paper equipped instrument when necessary. The following procedural outline refers to EEGs perform on the digital instruments. 1. If Instrument is not powered on, turn on system. Follow manufacturers instructions for initiating the EEG acquisition program. 2. Select PATIENT from the command bar; then select NEW. 3. Select PATIENT; then INFORMATION. Proceed to enter patient information, including MR#, name, EEG#, handedness, last meal, last sleep, medications, and pertinent history. 4. Measure and mark patient's head according to the 10-20 International system of measurement. Apply electrodes accurately and test impedances; impedances should be below 10 Kohm. 5. Instruct patient on behavior during EEG. Begin recording. 6. Beginning with the DB or Double Banana montage run 2.5 to 3 mins. of artifact free tracing for each montage including bipolar and referential montages. The montages are outlined on the following page. 7. Hyperventilation (HV) may be done early in the tracing in order to tire the patient preparatory to sleep, or later in the case of an older patient who should stay awake. If there are no contraindications to HV, record at least 1 min. of pre-HV, HV the patient for 3 minutes or more if necessary, and record at least 2 mins. postHV. HV should be recorded on the DB or "double banana" montage.

Rev 3/98

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS

STANFORD UNIVERSITY HOSPITAL EEG LABORATORY

8. Perform Photic Stimulation on the Photic montage. Photic frequencies to use are 1,3,6,9,12,15,18,21,24,27,30. Each frequency should be on for 10 secs. and off for 5 secs. The patient should be instructed to open and close their eyes on each frequency. An up and down sweep from 1 to 30 Hz should also be performed. Stop photic stimulation and protect the patient if the EEG or clinical observation suggests an impending seizure. 9. For Sleep EEG, patients should be encouraged to sleep for the majority of the recording, using sedation as necessary if ordered. For Awake/Sleep EEG a portion of both states should be recorded during the EEG. Sleep should be attempted in children and patients with seizures, suspected seizures, syncope and loss of consciousness. 10. Technologists will manipulate parameters (sensitivity, filter settings, paper speed, montage sequencing) to obtain the best recording as indicated by the EEG findings and patient history. 11. Annotations will be made by the technologist throughout the record using pre-set comments or "free comment" field to note patient state, movements, artifacts, and any other observation which will facilitate physician interpretation of the EEG. 12. At the end of the recording, enter the patient state seen during the recording field. 13. Clean the patient's head thoroughly. 14. If attached through the network connection, copy the EEG to the Review station for physician review. 15. Print out a Patient Information sheet and attach to billing form for physician.

Rev 3/98

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS

STANFORD UNIVERSITY HOSPITAL EEG LABORATORY III. Guidelines for Routine Activations During EEG

Routine activation with photic stimulation and hyperventilation should be performed on patients referred to the EEG lab for recording: Intermittent Photic Stimulation: 1. The patient should be instructed and reassured regarding photic stimulation. 2. Photic should be performed with the patient awake 3. The photic lamp should be eight (8) inches from the eyes, and the testing room darkened. Photic should be begun with the patient's eyes closed. 4. The patient should be stimulated at the following frequencies: 1, 3, 6, 9, 12, 15, 18 ,21 ,24 ,27 , 30 Hz. Each frequency should be on for 10 secs. and off for 5 secs. The patient should be instructed to open and close their eyes during each frequency. A crescendo-decrescendo flashing from 1 to 30 Hz. should also be performed. 5. If a photo-paroxysmal response is elicited the photic stimulation will be discontinued immediately; for confirmation, the frequency at which the patient is sensitive will be repeated briefly at least once. 6. Technologists should make themselves aware of the various disease entities and conditions in which intermittent photic stimulation is critical and/or useful. 7. CONTRAINDICATIONS: 1. When specifically ordered not to perform photic by the referring physician. 2. Immediately following cataract or other eye surgery.

Rev 3/98

POLICY AND PROCEDURE MANUAL: NEURODIAGNOSTIC LABS STANFORD UNIVERSITY HOSPITAL EEG LABORATORY Hyperventilation: 1. The patient should be instructed regarding hyperventilation (HV) and reassured about feelings of dizziness, lightheadedness, dry mouth, and feeling cold during the procedure. 2. Technologists will be aware of when HV produces a high yield of EEG abnormalities (i.e. absence seizures, etc.) and when it is not helpful. 3. HV should be performed with the patient in a sitting or reclining position with eyes closed. Respiratory rate should be 20-22 deep and regular breaths per minute for a minimum of 3 minutes. There should be a 1 min. baseline recording pre-HV and a minimum 2 min. post-HV recording. 4. The technologists will keep a close watch on the patient and be aware and make note of adverse clinical effects and/or clinical seizures or behavioral changes. If paroxysmal burst occur in the EEG recording the technologist should say a phrase (i.e. "pink elephant" or "yellow dog", etc.) to the patient during a burst to test the patients level of awareness at that time. At the end of HV the technologist should question the patient for memory of the phrase presented. The "Response Clicker" can be used as a substitute for the above procedure. 5. If a patient does not stop HV when asked to do so they should be asked to hold their breath for a few seconds or to breathe into a paper bag. When a patient has a severe adverse reaction to HV, have someone summon the nearest physician to examine the patient. DO NOT LEAVE THE PATIENT ALONE. 6. In patients where the chance of an abnormal response to HV is expected, every effort should be made to obtain at least some good HV breaths. 7. CONTRAINDICATIONS: I. Patients with respiratory difficulties, including those on 02, with COPD, asthma, etc. 2. When specifically ordered not to HV by the referring physician. 3. Patients immediately post-op (Fewer than 5 days) 4. Patients with known aneurysms. 5. Patients with acute CVAs or TIAs, or following recent MIs. 6. Pregnant women 7. Patients known to have severe uncontrolled hypertension 8. Patients known to have angina pectoris

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS STANFORD UNIVERSITY HOSPITAL EEG LABORATORY IV. Electrocerebral Silence (ECS) EEG Protocol The following protocol applies to EEG recordings for the determination of cerebral death. The protocol conforms to the guidelines of the American EEG Society for "Minimum Technical Standards for EEG Recording in Suspected Cerebral Death" (Journal of Clinical Neurophysiology 11(1): 10-13, Raven Press 1994) 1. Apply all standard electrodes according to the 10-20 system of placement, plus ground and EKG. Two additional electrodes should be applied to the dorsum of one hand separated by 6-7 cm. 2. Impedances should be under 10 kohms but over 100 ohms. 3. Calibrate and run Bio-Cal 4. Begin recording EEG using routine DB montage. If EEG is low voltage increase the amplification/sensitivity to better demonstrate the waveforms. 5. If after recording on the DB montage at increased amplification an EEG suggesting ECS is found the montage should be switched to one of the following appropriate montages: For recording on the digital Nicolet Voyageur instrument use: FP1-T3 T3-01 FP2-T4 T4-02 FP 1 -C3 C3-01 FP2-C4 C4-02 T3-CZ CZ-T4 FZ-PZ EKG Noncephalic LSO-AI RIO-A2 FPI-Al T3-Al 01-Al FP2-A2 F4-A2 02-A2 C3-Al C4-A2 FZ-Al PZ-A1 10Kohm-Resistor

Rev 3/98

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS STANFORD UNIVERSITY HOSPITAL EEG LABORATORY

When recording on paper equipped instrument use the following montage: 1. FP1-T3 9. T3-CZ 2. T3-01 10. CZ-T4 3. FP2-T4 11. FZ-PZ 4. T 4 - 0 2 12. EKG 5. FP I -C3 13. LSO-A1 14. RIO-A2 6. C3-01 15. Noncephalic 7. FP2-C4 16. 10Kohm Resistor 8. C4-02 With paper recordings use the following montage for the last 5 minutes of the EEG: 1. FPI-A1 9. FZ-A1 2. T3-A1 10. PZ-Al 3. 01-Al 11. EKG 4. FP2-A2 12. LSO-A1 5. T4-A2 13. RIO-Al 6. 02-A2 14. Noncephalic 7. C3-A1 15. 10Kohm Resistor. 8. C4-A2 6. Test the integrity of the recording system by touching each electrode in the montage gently with a pencil or cotton swab to create an artifact on the recording. Mark the tracing as each electrode is touched.

Rev 3/98

STANDARD EEG MONTAGES The following montages will be run on routine EEG recordings: CH # 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 DB FP1-F7 F7-T3 T3-T5 T5-01 FP2-F8 F8-T4 T4-T6 T6-02 FP1-F3 F3-C3 C3-P3 P3-01 FP2-F4 F4-C4 C4-P4 P4-02 FZ-CZ CZ-PZ LSO-Al RIO-A2 EKG IPSI EAR F7-A1 T3-A1 T5-Al 01-Al F8-A2 T4-A2 T6-A2 02-A2 F'P1-A F3-A1 C3-A1 P3-Al FP2-A2 F4-A2 C4-A2 P4-A2 FZ-A1 CZ-CZ-T4 PZLSO-A1 LSO-Al RIO-Al EKG PFOT FP1-F3 F3-C3 C3-T5-A1 P3-01-A1 FP2-F4 F4-C4 C4-P4 P4-02 F7FP1-A1 F3-FZ FZ-F4 F4-P3-A1 T5-P3 P3- PZ PZ- P4 P4-T6 F7-T3 T3-T5 T4LSO-A1 T4LSO-A1 LSRIO-A1 RIO-A2 EKG CIRCLE T3-F7 F7-FP I FP IFP2 FP2-F8 F8-T4 A1-T3 T3-C3 C3-CZ CZ-C4 C4-T4 T4-A2 T3-T5 T5-01 01T402-T6 T6-T4 F3-FZ FZ-F4 P3-PZ PZ-P4 LSO-Al RIO-A2 EKG TC P FP1-F7 F7-T3 T3-T5 T5-01 FP2-F8 F8-T4 T4-T6 T6-02 A 1 -T3 T3-C3 C3-CZ CZ-C4 C4-T4 T4-A2 FP1-F3 F3-C3 C3-P3 FP2-F4 F4-C4 C4-P3-T4 LSOT4-P4 RILSO-A1 EKG T I /T2 01-T5 T5-T3 T3-T1 Tl-FPI , FP1FP2 FP2-T2 T2-T4 T4-T6 T6-02 FP1-F3 F3-C3 C3-P3 P3-01 FP2-F4 F4-C4 C4-P4 P4-02 FZ-CZ CZ-PZ LSLSO-A1 T4LSO-A1 EKG PH OTIC FP I -F3 F3-C3 C3-P3 P3-01 FP2-F4 F4-C4 C4-P4 P4-02 T3-T5 T5-01 01-02 02-T6 T6-T4 A1-01 T3-01 C3-01 A2-01 T4-01 C4-01 LSOCZLSO-A1 21LSO-

Rev 3/98

POLICY AND PROCEDURE MANUAL EPILEPSY MONITORING SERVICES STANFORD HOSPITAL AND CLINICS I . General Policies 1. The Epilepsy Monitoring Unit (EMU) will perform long-term monitoring for epilepsy recordings to meet the "Guidelines for Long-Term Monitoring for Epilepsy" set forth by the American Society of Clinical Neurophysiology. (Journal of Clinical Neurophysiology 11(1):88-110, Raven Press, 1994) Long-term monitoring for epilepsy (LTME) refers to the simultaneous recording of EEG and clinical behavior over extended periods of time to evaluate patients with paroxysmal disturbances of cerebral function. LIME is used when it is important to correlate clinical behavior with EEG data. LTME is used to diagnose whether a patient is having epileptic seizures vs. some non-epileptic event, is used to characterize and classify seizures to procure the correct treatment type, is used to quantify the occurrence of seizures, and is used to assess appropriate patients for epilepsy surgery. Location: Stanford Hospital, Nursing Unit F3. Hours of operation: Patients monitored in the unit will be monitored continuously on a 24-hour basis. The number of days of monitoring will depend on the patients' clinical situation. Technologists from the Neurodiagnostic Labs Monday to Friday, 06:30 to 18:00 will staff the unit. The EMU is covered on an on-call basis from 18:00 to 06:30 and 24 hours a day on weekends. A monthly on-call schedule is provided to the hospitalpaging operator detailing the technologist on evening and weekend call. Patients are admitted to the EMU through the Stanford Comprehensive Epilepsy Center or by approval of one of the staff Epileptologists. The EMU will monitor both Phase I patients (surface electrode placement) and Phase II patients (surgically implanted electrode placement).

2.

3. 4.

5. 6.

POLICY AND PROCEDURE MANUAL EPILEPSY MONITORING SERVICES STANFORD HOSPITAL AND CLINICS II. Epilepsy Monitoring Protocol for Phase I Patients The following protocol applies to Phase I patient monitoring in the EMU. Both EEG data and video data of the patient will be recorded on a 24-hour basis on the Video/EEG system. EEG data will also be analyzed on-line by seizure detection software to aid in identifying questionably abnormal EEG events (spikes and/or seizures). 1. Power on both Video/EEG system and the Seizure Detection computer. Check parameters on the seizure detection program to ensure proper detection. 2. Input patient information into both Video/EEG system and the seizure detection computer. 3. Position camera on patient and start video tape recording as precaution to capture events during patient hook-up. 4. Greet and explain procedure to patient. 5. Measure and mark patient's head according to the 10-20 International system of measurement. The following electrodes should be applied and the order inputted into the system computers: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. FP 1 FP2 F3 F4 C3 C4 P3 P4 01 02 A1 A2 F7 14. F8 15. T3 16. T4 17. T5 18. T6 19. FZ 20. PZ 21 Empty input 22. TI (SPI) 23. T2 (SP2) 24. CZ 25. EKGI 26. EKG2

Apply electrodes accurately with collodian glue. Test impedances; impedances should be below 10 Kohm. 6. After electrodes are applied verify EEG data on Video/EEG system and the seizure detection computer. Select appropriate montage for monitoring. Adjust sensitivity, and/or filter settings as needed.
2

POLICY AND PROCEDURE MANUAL EPILEPSY MONITORING SERVICES STANFORD HOSPITAL AND CLINICS 7. When a satisfactory recording is seen on screen start the recording on the Video/EEG system using the manufacturers instructions. Start the spike and seizure detection recording on the seizure detection computer. 8. Wrap the patient's head with Kling gauze and Coflex stretch wrap to reduce movement artifacts and insure electrode attachment over extended periods of time. Place the preamplifier into a carrying pouch or wrap the preamplifier onto the top of the patient's head if they can tolerate it. 9. Instruct patient, family members, and patient sitters to squeeze the event bulb when a noted clinical event occurs. This will mark the event time on the videotape and signal the seizure detection computer to record data. 10. Have patient lie quietly for a period with segments of eyes closed and eyes open. 11. Perform 3 min of Hyperventilation with the patient lying quietly with eyes closed. Check for any contraindications for hyperventilation 12. Instruct patient on living with the wired telemetry hookup within the hospital room. Explain Do's and Don'ts concerning the monitoring procedure. 13. Patient is left alone to be monitored continuously by the recording systems. Patient will be monitored until adequate sampling of patient's events takes place. 14. Archive video and EEG segments of clinical interest to a long-term digital storage media, using HIPAA-compliant procedures.

POLICY AND PROCEDURE MANUAL EPILEPSY MONITORING SERVICES STANFORD HOSPITAL AND CLINICS III. Epilepsy Monitoring Protocol for Phase II Patients The following protocol applies to Phase H patient monitoring in the EMU. Both EEG data and video data of the patient will be recorded on a 24-hour basis on the Video/EEG system. EEG data will also be analyzed on-line by seizure detection software to aid in identifying questionably abnormal EEG events (spikes and/or seizures). 1. Power on both Video/EEG system and the Seizure Detection computer. Check parameters on the seizure detection program to ensure proper detection. 2. Input patient information into both Video/EEG system and the seizure detection computer. 3. Position camera on patient and start video tape recording as precaution to capture events during patient hook-up. 4. Greet and explain procedure to patient. 5. Verify implanted electrode placement through surgical map and electrode connector numbers. 6. Input electrode placement names into the computers. Create appropriate montage for monitoring with particular electrode set. 7. Set up sterile field at patient's scalp to attach electrode connectors to electrode cables. 8. Connect electrodes to appropriate cables and attach cables to the appropriate preamplifiers. 9. Have second technologist check for appropriate connections of electrodes, cables, and preamplifiers as verification. 10. Verify recording on screen for all electrode placements using referential input montage. Switch to specific bipolar montage for this particular patient's monitoring. Adjust parameters to obtain best recording on screen. 11. When a satisfactory recording is seen on screen start the recording on according to the manufacturers specifications. Start the spike and seizure detection recording on the seizure detection computer. 15. Wrap the patient's head with kling gauze and Coflex stretch wrap to reduce movement artifacts and insure electrode attachment over extended periods of time. Place the preamplifiers into a carrying pouch and secure to the bed. 16. Instruct patient, family members, and patient sitters to squeeze the event bulb when a noted clinical event occurs. This will mark the event time on the videotape and signal the seizure detection computer to record data.

POLICY AND PROCEDURE MANUAL EPILEPSY MONITORING SERVICES

STANFORD HOSPITAL AND CLINICS

17. Have patient lie quietly for a period with segments of eyes closed and eyes open if they are able to cooperate. 18. Instruct patient on living with the wired telemetry hookup within the hospital room. Explain Do's and Don'ts concerning the monitoring procedure. 19. Patient is left alone to be monitored continuously by the recording systems. Patient will be monitored until adequate sampling of patient's events takes place. Archive video and EEG segments of clinical interest to a long-term digital storage media, using HIPAA-compliant procedures.

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS

STANFORD HOSPITAL AND CLINICS INTRAOPERATIYE MONITORING SERVICE I. General Policies 1. The Intraoperative Monitoring Service of the Neurodiagnostic Labs will conform to the Guidelines for Intraoperative Monitoring of Sensory Evoked Potentials established by the American Clinical Neurophysiology Society (formerly the American EEG Society). ( Journal of Clinical Neurophysiology 11(I):77-87 Raven Press, 1994) 2. The Intraoperative Monitoring Service provides information regarding a surgical procedure's effect upon a patient's central and peripheral nervous systems. IOM is used to assess the functional state of the sensory pathways in patients undergoing neurosurgical, vascular or orthopedic surgical procedures. The expected outcome of the monitoring is to preserve or improve a patient's presurgical neurological function. 3. The IOM service will provide monitoring of Somatosensory Evoked Potentials(SEP) (upper and lower extremities), Brainstem Auditory Evoked Responses (BAER), continuous EEG, Transcranial Doppler studies (TCD), and cranial nerve EMU. The particular modalities to be monitored for each surgical case are determined by the director of the monitoring service or the IOM fellow in consultation with the surgeon performing the case. 4. The director of the service will consult with the anesthesiologist in each case in selecting the appropriate anesthesia to insure maximal patient safety with minimal influence on the monitored modalities. 5. Patients will be monitored by qualified END Technologists who demonstrate competencies in Intraoperative Monitoring. 6. Patients will be setup for monitoring with appropriate recording and stimulating electrodes. Recording electrodes will be applied with collodian. Electrode gel will be utilized to reduce impedances between the electrodes and the patients scalp. The blunted applicator used for gel application will only be used on one patient and then discarded in an appropriate sharps container. Electrode impedances should be less than 5K ohms.

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS STANFORD HOSPITAL AND CLINICS INTRAOPERATIVE MONITORING SERVICE

7. Baseline recordings will be established on all patients following induction of anesthesia and positioning of the patient prior to surgery start. These recordings will be used throughout the surgery to establish degree of change in the recorded activities. 8. Monitoring will be continuous through the procedure. Trace recordings will be performed every 10 minutes during non-critical surgical time. Trace recordings will be performed continuously during critical surgical manipulation times. 9. Anesthesia % levels, Mean Arterial Pressure (MAP), and temperature will be noted for each tracing recorded. 10. An interpreting physician neurophysiologist will be physically present for all critical surgical manipulations. At other times he will be immediately available if needed. All interpretations, recommendations and decisions regarding actions or consequences are to be made by the physician neurophysiologist. 11. Monitoring and recording will continue to the end of the surgical procedure. 12. Post surgery surface electrodes will be rinsed in hospital approved disinfectant after each O.R. case. If contaminated with blood they will be rinsed in disinfectant and then sent to supply processing for gas sterilization. EMG needles will be disposed of according to procedures for disposal of such items.

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS STANFORD HOSPITAL AND CLINICS INTRAOPERATIVE MONITORING SERVICE II. Electrode Setups and Montages I. Internal Carotid Surgery For surgery requiring the assessment of the cerebrum during internal carotid surgery continuous EEG, median nerve somatosensory evoked potentials and TCD are monitored. The following electrodes should be applied: CZ F3 C3 F4 C3' FZ C4 L Erbs point C4' R Erbs point P3 Linked Ears P4 C7

Note: Electrode positions are measured according to the 10-20 International System of Placement. C3' and C4' are measured 2 cm. behind C3 and C4. The following montage should be recorded: CH I F3 - Linked Ears CH 2 C3 - Linked Ears CH 3 P3 - Linked Ears CH 4 F4 - Linked Ears CH 5 C4 - Linked Ears CH 6 P4 - Linked Ears CH 7 C4'- FZ CH 8 C3'- FZ Stimulating electrode bars are applied to the inferior surface of each wrist to stimulate the median nerve. In addition the middle cerebral artery (MCA) on the side of the surgery is monitored with Transcranial Doppler (TCD) for the generation of emboli
.

POLICY AND PROCEDURE MANUAL

NEURODIAGNOSTIC LABS

STANFORD HOSPITAL AND CLINICS INTRAOPERATIVE MONITORING SERVICE 2. Spinal Cord and Non Posterior Fossa AVM And Tumors For surgery requiring the assessment of the somatosensory pathways in the spinal cord and/or the cerebrum upper and lower somatosensory evoked potentials should be monitored. The following electrodes should be applied: CZ CZ' C3' C4' FZ C7 L Erbs point R Erbs point Note: Electrode positions are measured according to the 10-20 International System of Placement. C3', C4', and CZ' are measured 2 cm. behind C3, C4, and CZ respectively. The following montage should be recorded: CH I CH 2 CH 3 CH 4 CH 5 CH 6 CH 7 CH 8 C3'-C4' FZ - C3' C4'-C3 FZ - CZ'

C4'- C3' FZ - CZ' C3'- C4' L median stimulation R median stimulation R median stimulation L tibial stimulation L tibial stimulation R tibial stimulation R tibial stimulation Stimulating electrode bars are applied to the inferior surface of each wrist to stimulate the median nerve and to the inside surface of the ankle to stimulate the tibial nerve.

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS STANFORD HOSPITAL AND CLINICS INTRAOPERATIVE MONITORING SERVICE 3. Posterior Fossa and Brainstem AVM and Tumors For surgery requiring the assessment of the somatosensory pathways in the cerebrum and the auditory brainstem pathways median somatosensory and auditory evoked potentials should be monitored. The following electrodes should be applied: CZ A1 A2 C3' C4' FZ C7 L Erbs point R Erbs point

Note: Electrode positions are measured according to the 10-20 International System of Placement. C3', C4', and CZ' are measured 2 cm. behind C3, C4, and CZ respectively. The following montage should be recorded: CHI CZ - A1 L BAER CH 2 FZ - C4' L median stimulation CH 3 C3'- C4' L median stimulation CH 4 L ERBS- FZ L median stimulation CH 5 CZ - A2 R BAER CH 6 FZ - C3' R median stimulation CH 7 C4'- C3' R median stimulation CH 8 R ERBS-FZ R median stimulation Stimulating electrode bars are applied to the inferior surface of each wrist to stimulate the median nerve. Ear insert phones are placed for auditory stimulation.

POLICY AND PROCEDURE MANUAL EPILEPSY MONITORING SERVICES STANFORD UNIVERSITY HOSPITAL WADA PROTOCOL I. PURPOSE The Wada Study (Intracarotid Dominance Study) is used to: A. determine the lateralization of language and memory prior to resective surgery or corpus callosotomy. B. aid in the localization of the epileptogenic focus. H. RESPONSIBILITY FOR THIS POLICY The Director of the Stanford comprehensive epilepsy center is responsible for establishing this protocol, in conjunction with the Chief of Neuroradiology. HI PROCEDURE A. Patients are scheduled with the Department of Neuroradiology , Angiogram division by the Comprehensive Epilepsy Center. B. Patients are admitted the morning of the Wada/angiogram to the Ambulatory Treatment Unit at 6:30 a.m. 1. Patients are to be NPO after midnight on the day of the procedure 2. Patients are not to receive any sedation prior to the procedure. C. Patients are hooked up for EEG monitoring during the Wada with standard EEG placements measured by the 10-20 International System of measurement. Electrodes are applied with paste and the patient's head is wrapped with conforming bandage to insure electrode contact through the study. D. The following montage is run on the EEG for the study: 1. FPI - F7 9. FP2 - F8 17. T3 - C3 2. F7 - T3 10. F8 - T4 18.C3 - CZ 3. T3 - T5 11. T4 - T6 19. CZ - C4 4. T5 - 01 12. T6 - 02 20. C4 - T4 5. FP 1 .- F3 13. FP2 - F4 6. F3 - C3 14. F4 - C4 7. C3 - P3 15. C4 - P4 8. P3 - 01 16. P4 - 02

POLICY AND PROCEDURE MANUAL EPILEPSY MONITORING SERVICES STANFORD UNIVERSITY HOSPITAL WADA PROTOCOL E. THE SIDE OF THE EPILEPTOGENIC FOCUS WILL BE INJECTED FIRST. Once the angiogram has been completed on this side, the Wada will begin: I. Sodium Amytal 125mg in 5cc will be drawn up in the syringe. An additional 50 mg in 2cc will be drawn up and available if needed. 2. Injection of Amytal 125mg will take place over 4 seconds. 3. If no hemiparesis is induced, then the additional 50mg of amytal will be given. 4. Continuous EEG recording will be obtained from at least 2 minutes prior to injection, through stimulus presentation and test of recall. Paper speed may be changed to 15mm/sec. once stimulus presentation is complete 5. Where amobarbital is unavailable, alternative agents, for example methohexital (Brevital) may be used, with injections of from 2-6 (typically 5) mg intra-carotid F. The catheter will be repositioned to the opposite internal carotid. Once the angiogram has been completed the Wada will begin on this side: 1. The above process will be repeated for the second side. 2. As clinically indicated, Wada testing may be performed only on one carotid in some cases. G. Once the procedure is completed the patient will remain in the hospital for post angiogram nursing care for a minimum of 4 hours.

DEPARTMENT OF NEUROLOGY AND NEUROLOG1CAL SC1ENCES

STANFORD UNIVERSITY MEDICAL CENTER

BOTULINUM TOXIN POLICY AND PROCEDURES NE U RODIAGNOSTIC LABS

Patients receiving Botulinum injections in the Neurodiagnostic Labs are seen for initial evaluation by the performing neurologist prior to first injection. A history is obtained and examination performed. The patient is advised of the benefits, risks and side effects of the medication prior to first injections. Botulinum injections performed in the Neurodiagnostic Labs are performed for medically indicated conditions only, including but not limited to torticollis, dystonia, blepharospasm, hemifacial spasm, and spasticity. Injections are performed in the Neurodiagnostic Labs. Medication is stored in a refrigerator/freezer located in Room H-3136 and kept in accordance with manufacture's specifications. A daily temperature log is maintained. Any outdated medication is returned to the pharmacy for disposal. The injections are performed using sterile technique and mixed according to the manufacture's specifications. Medication that is not used is destroyed under Stanford Hospital and manufacturer's guidelines. When medically indicated Botulinum toxin injections are performed under EMG guidance. Following injections the patient remains in the Neurodiagnostic Lab for 15-30 minutes to monitor for any side effects from the medication. Patients are advised to contact the treating physician should there be any side effects noted. Re-treatment is performed when patients note return of symptoms, however, not prior to three months from previous treatment according to the manufacture's guidelines. Records are maintained in the Neurodiagnostic Lab including a Botulinum Toxin worksheet indicating muscles injected and amounts given. A separate log is maintained for any studies being performed using Botulinum Toxin A and B. Informed consent is obtained and copies are kept by the study coordinator. Separate temperature logs are maintained as well as patient and injection site information. Further information may be obtained by contacting the Neurodiagnostic Labs at 7236888. Updated 7/26/2010

DEPARTMENT OF NEUROLOGY AND NEUROLOGICAL SCIENCES

STANFORD UNIVERSITY MEDICAL CENTER

Stanford University Hospital and Clinics L ucille Salter Packard Children's Hospital 300 Pasteur Drive, Rm. A343 Stanford, CA 94305-5235

BOTULINUM TOXIN TREATMENT Description: Botulinum toxin blocks the release of acetylcholine from the motor nerve ending causing a chemical denervation of muscle. There are two types of Botulinum toxins that have been approved by the Food and Drug Administration (FDA): Botulinum toxin type A (Botox ) and Botulinum toxin type B (Myobloc). Clinical Effects: Muscle weakness and/or paralysis of targeted muscles. Clinical Indications: Botulinum toxin is utilized in the treatment of the following disorders; movement disorders, which include blepharospasm, hemifacial spasm, spasmodic torticollis, cervical dystonia, spasmodic dysphonia, limb dystonias, and other focal dystonias. Botulium toxin has also been reported to be useful in the treatment of headaches, spasticity, and low back pain. Both Botulinum toxin type A and B have been approved by the FDA for the treatment of cervical dystonia. In addition, Botulinum toxin type A has FDA approval for the treatment of strabismus, facial nerve disorders, and frown lines. Stanford Protocol: When patients are first evaluated for possible Botulinum toxin treatment, the physician should determine the appropriate course of therapy based upon the patient characteristics, diagnosis, and response to previous treatment. If the determination is made that Botulinum toxin therapy is to be initiated, the type of Botulinum toxin and the proper dose will be determined based upon the patient's symptomatology. Potential side effects as described in the prescribing information for Botox or Myobloc are discussed with the patient prior to the initiation of therapy. Treatment may or may not be performed using electromyographic guidance.

WHAT IS BOTULINUM TOXIN? Botulinum toxin is a powerful poison that is made by a bacterium, called clostridium botulinum. The effect of the toxin is to weaken or paralyze muscle by interfering with the message that the nerve gives to the muscle to contract. Outbreaks of botulism have occurred associated with the consumption of improperly preserved foods. The problem arises when the food is canned or jarred such that the bacteria grow and produce the toxin. When the improperly preserved food is eaten, the toxin is absorbed into the bloodstream and causes weakness of the muscles, including the muscles for breathing. The weakness is temporary. The botulinum toxin used in clinical practice is purified so there are no bacteria or other contaminants. The doses recommended to treat spasmodic torticollis are well below doses that could cause human botulism. Overall, botulinum toxin has been found to be a safe and effective treatment for a variety of disorders, including spasmodic torticollis. HOW DID BOTULINUM TOXIN COME TO BE USED AS A MEDICATION? The idea that localized injections of small amounts of botulinum toxin may relieve medical disorders associated with involuntary activation of muscles was pioneered by Dr. Man Scott in the early 1980's. Dr. Scott found that by injecting tiny amounts directly into eye muscles, the symptoms of strabismus (lazy eye) could be improved. He then proceeded to try the toxin in a condition called blepharospasm. Blepharospasm is an involuntary spasm of the muscles around the eye such that the eyes blink excessively or become squeezed closed, sometimes rendering a person functionally blind. Injections of botulinum toxin into these overactive muscles around the eye resulted in a relaxation of the muscles and an improvement of the symptoms, restoring almost normal function to many patients with this problem. Subsequently, botulinum toxin was used to treat other disorders in which abnormal muscle activity was causing the symptoms. Botulinum toxin was initially used in patients with spasmodic torticollis in 1984 and has subsequently been shown in many studies to be a safe and effective treatment.

DOES BOTULINUM TOXIN TREATMENT CURE SPASMODIC TORTICOLLIS? No. The origin of spasmodic torticollis is believed to be located in the lower part of the brain, causing a message to be sent from the brain to the neck muscles telling them to contract. The end result is that the muscles are abnormally activated causing the neck and head to turn. Botulinum toxin, when injected into a muscle, interrupts this message, thus relaxing the overactive muscles and allowing the head and neck to be in a more normal position. The underlying problem, however, has not been treated. The effects of the toxin last about 3-4 months on average. After that time, the message from the brain again reaches the neck muscles and the symptoms return. HOW LONG DOES BOTULINUM TOXIN TAKE TO ACT AND WHAT IS THE LENGTH OF THE RELIEF? The effect of the toxin usually begins in about three days after the injection. There is a gradual relaxation of the injected muscles, usually reaching a peak 2-4 weeks after treatment. The benefit remains fairly stable for about 2-3 months, at which time the effect gradually wears off and the symptoms slowly return. Therefore, patients are usually re-injected every three to four months. HOW MANY PATIENTS HAVE BEEN INJECTED AND HOW MANY BENEFIT? Thousands of patients with spasmodic torticollis have received the botulinum toxin injections. Approximately 75% to 85% obtain some relief of pain and improvement of head position. The injections do not usually completely alleviate the symptoms, but provide for substantial improvement.

WHAT ARE THE SIDE EFFECTS FROM BOTULINUM TOXIN INJECTIONS? At the time of injection, there may be pain or bruising from the needle inserted to inject the toxin. In the first two weeks following injection, some patients have noticed new pain in the neck muscles. This pain likely originates from the shrinkage of the injected muscles or from other muscles that may be trying to make up for the effects of the toxin. Usually, using mild analgesics such as acetaminophen, cool compresses, and sometimes a soft collar will alleviate this pain. The pain typically lasts from Ito 3 weeks and then goes away. Swallowing problems have also been reported in up to one-third of the patients following botulinum toxin treatment and are likely due to the spread of small amounts of the toxin to the swallowing muscles. The swallowing problem consists of a feeling that coarse solid foods, such as bread, chips, or steak, get caught in the throat and that one must swallow a few times, or drink water in order to clear the throat. This side effect typically is mild, beginning 3 to 10 days following treatment and lasting from l to 3 weeks, although a few patients have had the symptoms for up to 6 weeks. Avoiding large chunks of coarse solid foods during the time of the swallowing discomfort is the best course of action. If swallowing symptoms are more severe, contact your physician. Sometimes, following the botulinum toxin injections, there can be some neck weakness. This may be noticed when leaning forward or when rising out of bed. This weakness is usually described as a heavy feeling of the head. Usually, signs of weakness occur about two weeks following injection and last a variable amount of time, sometimes as long as a few weeks but then completely resolving. If bothersome, wearing a soft neck collar can be of some help in relieving the symptom. Another side effect reported in a very small number of patients include a temporary feeling of generalized tiredness or flu-like symptoms lasting a couple of days. No patient has ever gotten botulism from these treatments because of the very small doses used. If you have side effects that are not mild, you should notify your doctor. HOW IS THE BOTULINUM TOXIN TREATMENT GIVEN? The botulinum toxin is injected with a needle directly into the overactive neck muscles. In order to do this, the doctor will have you sit in a chair in a relaxed position and will stand behind you. Many doctors use an electromyograph, which is a machine that measures muscle activity, to select the muscles to be injected. Others select the muscles by examining the abnormal head position and feeling for muscle spasm. The botulinum toxin, which is packaged in a small vial, is diluted with a small amount of sterile salt water and put into a small syringe attached to a fine needle. If the doctor uses the electromyograph to select muscles for injection, the needle used is one that can be attached to the machine to record the muscle activity and is hollow, allowing injection directly through the needle. The needle is inserted into several muscles and the doctor watches and listens for the characteristic muscle activity. This may appear on the screen or may be heard through an amplifier and speaker as a rumbling or thunder-like noise. Sometimes, based on this activity, the doctor will choose not to inject botulinum toxin into the particular muscle, but rather to search for other more active muscles. An entire treatment usually can be completed in less than 30 minutes. You will be able to get up immediately after the injections and resume your normal activities. If you have just been treated with botulinum toxin for the first time, you may be asked to return to the office two to four weeks following the initial injection in order to evaluate the outcome and side effects from the injections. 'Some doctors may administer "booster" injections at the time of the follow-up visit if the response has been inadequate.

At the end of three to four months if the toxin has begun to wear off and symptoms are returning, an appointment for another injection is usually made. WILL THE INJECTIONS BECOME LESS EFFECTIVE OVER TIME? Repeated injections of hotulinum toxin have caused resistance to the toxin in some patients. This means that after several treatments with good results, the injections may lose their effect. Fortunately, the development of resistance to botulinum toxin is unusual, affecting only a small number of people. It appears that frequent treatments (at intervals less than 3 months), routine use of "booster" injections and high doses of toxin predispose to the development of resistance. Limiting the dose of botulinum and the frequency of treatments is viewed as the best way to avoid development of resistance. Some doctors check a blood test to see if the patient has developed an immunity to the toxin because of botulinum toxin antibodies, but accuracy of this test in identifying patients who are resistance is unproven, thus the usefulness of this test is unknown. Sometimes, the doctor will perform a special test to check for botulinum toxin resistance Newer tbrms of hotulinum toxin (botulinum toxin serotype B and F) have been studied in patients who have become resistant to the approved form of the toxin (type A). Many patients who are resistant to type A will respond to type B. DOES INSURANCE OR MEDICARE COVER THE COST OF THE BOTULINUM TOXIN INJECTIONS? Medicare has approved the botulinum toxin injections for spasmodic torticollis. If you have private insurance or an HMO, you should check with your insurance company regarding coverage. Last update: 7/20/2010

BOTOX' (Botulinum Toxin Type A)

Purified Neurotoxin Complex
Description: BOTOX (Botulinum Toxin Type A) Purified Neurotoxin Complex is a TTerile, vacuum-dried purified botrilinum toxin type A. produced from fermentation of Hall strain Clostridium botulinum type A grown in a medium containing casein hydrolysate, glucose and yeast extract It i s purified from the culture solution by dialysis and a series of acid precipitations to a complex consisting of the neurotoxin, and several accessory proteins. The complex Is dissolved in 'sterile sodium chloride solution containing albumin human and is sterile filtered (0.2 m icrons( prior to filling and vacuum-drying. One unit (U) of BOTO corresponds to the calculated median mtraperitoneal lethal dose LUst) in mice. The method utilized for performing the assay is specific to Allergan's product, BOTO. Due to specifi c details of this assay such as the veh icle, dilu tion scheme and laboratory protocols for the various mouse CDs assays. Units of biological 'cavity of BOTOX cannot be compared to nor converted into Units of any other botulinum toxin or any toxin assessed with any other specific assay method. Therefore, differences in species sensitivities to different botulinum neurotoxin serotypes precludes extrapolation of animal-dose activity relationships to human dose estimates. The specific activity of BOTOr is approximately 20 units/sonogram of neurotoxin protein complex. Each vial of BOTO contains 100 units (U) of Clostridium botulinum type A neurotoxin complex, 0.5 milligrams of albumin (human), and 0.9 milligrams of sodium chloride in a 'sterile. vacuum-dried form without a preservative, Clinical Pharmacology: BOTOX blocks neuromuscular transmission by binding to acceptor sites on motor nerve terminals, entering the nerve terminals, and inhibiting the release of ace ty l c h o l i n e . Th i s i n h i b i ti o n o c c u r s as th e n e u rotox in cle ave s S NAP-2 5 , a prote i n integral to the successful docking and release of acetylcholine from vesicles situated within nerve endings. When infecte d intramuscularly at therapeutic dos es, BOTO produces partial chemical denervation of the muscle resulting in a localized reduction in muscle activity. In addition, the muscle may atrophy, axonal sprouting may occur, and extrajunctional acetylcholine receptors may develop. There is evidence that reinnervation of the muscle may occur, thus slowly reversing muscle denervation produced by BOTOX. Pharmacokinetics Botulinum Toxin Type A is not expected to be present in the peripheral blood at measurable levels following IM injection at the recommended doses. The recommended quantities of neurotoxin administered at each treatment session are not expected to result in systemic, overt distant clinical effects, re, muscle weakness. in patients without other neuromuscular dysfunction. However, sub-clinical systemic effects have been shown by single-fiber electromyography after IM doses of botulinum toxins appropriate to produce clinically observable local muscle weakness. Clinical Studies: Cervical dystonia: A phase 3 randomized, multi -cente r, double blin d, placebo-controlled study of th e treatment of cervical dystonia was conducted! This study enrolled adult patients with cervical dystonia and a history of having received BOTO in an open label manner with perceived good response and tolerable side effects_ Patients were excluded if they had previously received surgical or other denervation treatment for their symptoms or had a known history of neuromuscular disorder. Subjects participated in an open label enrichment 'period where they received their previously employed dose of BO TOX O nly patients .vho were again perceived as showing a response were advanced to the randomized -'valuation period. The muscles in which the blinded study agent truectrons were to be administered ware determined on an individual patient basis. There were 214 subiects evaluated for the open label period, of which 170 progressed into Me randomized, blinded treatment period (88 in the BOTO group, 82 in the placebo ;coup). Patient evaluations continued for at least 10 weeks post-I/glee/lora The primary mtcome for the study was a dual endpoint. requiring evidence of both a change in the Cervical Dystonia Severity Scale (CDSS) and an increase in the percentage of patients :bowing any improvement on the Phy sicians Global Assessment Scale at 6 weeks afte r ne i n l e C t l O g session. The CUSS quan tif ies the severity of a b n o r m a l head posi tioning an d pas newly devised for this study. CUSS allots I point for each 5 degrees (or part thereof) of lead deviation in each of the three planes of head movement !range of scores up to tn e ore ti cal max i mu m of 54 1 Th e Phy s i ci an G l obal Asse s s m en t S cal e is a 9 cate gory :cafe scoring the physician's evaluation of the patients' status compared to baseline. :ringing from -4 to +4 (very marked worsening to complete improvement). with 0 indicating no change from baseline and +1 slight improvement. Pain is also an important symptom al cervical dystonia and was evaluated by separate assessments of pain frequency and .everay on scales at U (no pain) to 4 (constant in frequency or extremely severe in intensity). Ptudy results on the primary e n d p o i n t s and the pain-rel ate d secondary endpoin ts are :hewn in Table 1.

Manufactured by. Allergen Pharmaceuticals (Ireland) Ltd. a subsidiary of: Allergan, Inc,. 2525 Dupont Dr.. Irvine, CA 92612

Table I. Efficacy Outcomes of the Phase 3 Cervical Dystonia Study ;Group Means(
Placebo N-82
1

BOTOX.
N-88 92 I 3 51%

15. CI on Difference
T T

ft theline CUSS Ma n ge in C D S S at W eek 6 Percentage Patients with Any Improvement on Physicians Global Assessment P tin Intensity Baseline Change in Pain Intensity at W eek 6 Pain Frequency Baseline Change in Pain Fr equenc y at W eek 6

t3 it 3 11,

P2 3. 0 3/ t5 5 9

15

18 -n4 fa7 U 'I

13

lS

fl a

n3

409

I' I9 Those values

Irollps

represent the prospectively planned method for meet data imputation and statistical test a n a ry s e s in di c a t e d th a t th e 9 5S ti c o n l i d en e in t erv a l e xc l u de d th e v a lu e o f n o d iff e r enc e b etw e e n and the p-value was less than 0 05 These analyses included several alternative M I SSM Q data ;reputation rettleods and non parametric; Statistical lasts . I confidence intervals are based on the trdistributIOn

C onf i d enc e in t er v a l s ar e (( instr uc ted fr om the arm ies of c ovar ianc e able a & t r e at m en t a n d i nv es t i g a tio n 'e as main (reacts and baseline CDSS as a caeca e

Exploratory analyses of this study suggested that the majority of patients who had shown a benetrotal response by week 6 had returned to their baseline status by 3 months after treatment. Expl oratory analyses of s ubsets by patien t sex and age sugge st th at both sexes receive benefit, although female patients may receive somewhat greater amounts than male patients. There is a consistent treatment-associated effect between subsets greater than and less than age 65 (see also Precautions: Geriatrics). There were too few non-Caucasian patients enrolled to draw any conclusions regarding relative efficacy in racial subsets. There were several randomized studies conducted prior to the phase 3 study which were supportive but not adequately designed to assess or quantitatively estimate the efficacy of BOTO. In Me phase 3 study the median total BOTO dose in patients randomized to receive BOTOX (n=88) was 236 U. with 25th to 75th percentile ranges of 19810 300 U. Of these 88 patients. most received injections to 3 or 4 muscles: 38 received iniections to 3 muscles. 28 to 4 muscles. 5 to 5 muscles and 5 to 2 muscles. The dose was divided amongst the affected muscles in quantities shown in Table 2. The total dose and muscles selected were tailored to meet individual patient needs. Table 2: Number of Patients Treated Per Muscle and Fraction of Total Dose Injected into Involved Muscles
M uscle'

Number of Patients Treated in this Muscle (N=88)

43

Mean % Dose per Muscle

mid-Range of % Dose per Muscle'

25-90

Splenius capes/cervices s ter n oc l e i dor n as t e d t eva to r scapulae

I meezins iemispinarIS

P-R

77

:7-31
1 Si 25

19

13-33 I 3 25

Scalene I crigissimes

15 d

5-21 t 7 41

Pm mid-range of dose is calculated as the 25th to 75th percentiles . ` l or e . T h er e wer e 1 6 p at i en ts wh o h a d a dd i ti on a l m us c les inf ec t ed .

Blepharospasm: Potulinum toxin has been investigated for use in patients with blepharospasm in several studies. In an open label uncontrolled study, 27 patients with essential blepharospas m -'ere injected with 2.0 U of ecno at each of six sites on each side. One patient had not received any prior treatment. Twenty-six of the patients had not responded to therapy with nenztropine mesylate, clonazepam and/or bacloten. Three of the 26 patients continued to txperience spasms following muscle stripping surgery. Twenty-five of the 27 patients treated with botulinum toxin reported improvement within 48 hours. One patient was controlled with a higher dosage at 13 weeks post initial injection and one patient reported mild improvement but remained functionally impaired. 2 In another study, 12 patients with blepharospasm were evaluated in a double-blind, placebo:ontrolled study. Patients receiving botulinum toxin (n=8) improved compared with the placebo group (n=4). The mean dystonia score improved by 72%, the self-assessment core rating improved by 61%, and a videotape evaluation rating improved by 39%. The , :elects of the treatment lasted a mean of 12.5 weeks. One thousand six hundred eighty-four patients with blepharospasm who were evaluated n an open label trial showed clinical improvement as evaluated by measured eyelid force and clinically observed intensity of lid spasm. lasting an average of 12.5 weeks prior to the :seed for re-treatment.

Stanford University Medical Center

Botulinum Toxin Thera Pro ress R d

STANFORD MEDICAL CENTER NEUROPSYCHOLOGY SERVICE POLICY AND PROCEDURES

The Stanford Neuropsychology Service is located in the Neurodiagnostic Laboratory in the Department of Neurology and Neurosciences. We serve adults and adolescents from within the Stanford health care system and from the community. Services provided include neuropsychological evaluations and psychological assessments. We also provide brief focused psychotherapy for a small group of patients we have evaluated; treatment is primarily educational in nature. The population served consists of individuals with a wide range of disorders including traumatic brain injury, dementia, Parkinson's, epilepsy, immune disorders, stroke, brain tumors, attention deficit hyperactivity disorder, learning disabilities, and psychiatric conditions. Neuropsychological testing involves the evaluation of patients using standardized instruments sensitive to the behavioral, emotional and cognitive correlates of cerebral dysfunction. A battery of neuropsychological tests is administered in a standardized fashion and interpreted with a normative database. A typical evaluation involves a clinical interview and testing of: concentration, learning and memory; language-based abilities such as verbal fluency, and receptive and expressive speech; visual spatial abilities; fine motor speed; abstract reasoning and other cognitive abilities relevant to the specific referral question. When appropriate, psychological or personality assessment is conducted. Evaluations are used to clarify diagnostic questions and treatment options, as follows: 1) Determine if a patient suffers from neurocognitive dysfunction 2) Clarify the nature and severity of the disorder 3) Provide a baseline for longitudinal follow-up, i.e., document the course of a dementing disorder, recovery from a brain injury or surgical procedure. 4) Determine mental capacity for independent living or return to work/school 5) Identify psychological factors such as depression that contribute to cognitive dysfunction 6) Facilitate rehabilitation by evaluation of cognitive strengths and weaknesses 7) Provide treatment recommendations and referrals 8) Provide education and brief counseling for adjustment to cognitive disability The patients evaluated have a wide range of disorders, but the Neuropsychology Service also has some specialty programs linked to particular clinics in the Department of Neurology. The Movement Disorders Clinic and the Comprehensive Epilepsy Service require that their patients undergo neuropsychological testing in order to determine suitability for surgical intervention. Each program has a Lead

Neuropsychology Service P o l i c y a n d P r o c e d u r e s Page 2 of 3

Neuropsychologist who provides a tailored battery to assess cognitive status and psychological adjustment. Neuropsychological testing takes approximately four hours for patients with Parkinson's disease who are being considered for deep brain stimulation. The patient and usually a family member are interviewed. The following is a list of tests in the typical battery: Wechsler Test of Adult Reading Animal Naming Test Boston Naming Test FAS Letter-word Fluency Trail Making Test Wechsler Abbreviated Scale of Intelligence Scale (WASI) Wechsler Memory Scale-III (Selected subtests) Mattis Dementia Rating Scale-II Beck Anxiety Inventory Beck Depression Inventory Frontal Systems Behavior Scale (FrSBe) Parkinson's Disease Quality of Life Questionnaire Patients with mesial temporal lobe epilepsy who are being considered for a temporal lobectomy undergo a six to seven hour battery. In addition to interviews, this battery usually includes the following tests: Wechsler Test of Adult Reading Wechsler Abbreviated Scale of Intelligence (WASI) Wechsler Memory Scale-III (WMS-III) California Verbal Learning Test-II (CVLT-II) Brief Visual Memory Test-Revised Hooper Visual Organization Test Judgment of Line Orientation Auditory Responsive Naming Boston Naming Test FAS Animal Naming Multilingual Aphasia Examination (MAE; Token Test, Sentence Repetition Test0 Delis-Kaplan Executive Functioning System (D-KEFS; Design Fluency) Trail Making Test Stroop Test Wisconsin Card Sorting Test Beck Depression Inventory-II (BDI-II) Beck Anxiety Inventory

Neuropsychology Service P o l i c y a n d P r o c e d u r e s Page 3 of 3

The Stanford Center for Memory Disorders is co-directed by Neurology and Neuropsychology. The test battery for these patients is designed to assist in differential diagnosis and is used with patients referred with a question of MCI, Alzheimers Disease, Frontotemporal Dementia, Lewy Body Dementia and Parkinsons Plus conditions. The battery usually takes four hours and in addition to interviews usually consists of the following: tests: Wechsler Test of Adult Reading (WTAR) Wechsler Abbreviated Scale of Intelligence (WASI) Wechsler Adult Intelligence Scale-III (WAIS-III; Coding) Hopkins Verbal Learning Test-Revised (HVLT-R) Brief Visuospatial Memory Test-Revised (BVMT-R) Wechsler Memory Scale-III (WMS-III; Digit Span, Logical Memory I/II) Multilingual Aphasia Examination (MAE; Token Test, Sentence Repetition Test) Pyramids & Palm Trees Boston Naming Test (30-item version) Hooper Visual Organization Test (15-item version) Judgment of Line Orientation (20-item version) Repeatable Battery for the Assessment of Neuropsychological Status -Figure Copy Clock Drawing Test Wisconsin Card Sorting Test Trail Making Test Victoria Stroop Test Category Fluency Letter Fluency Grooved Pegboard Test Geriatric Depression Scale (30-item) Frontal Systems Behavior Scale (FrSBe) Family rating Functional Assessment Questionnaire (FAQ) The Neuropsychology staff consists of licensed clinical psychologists, with advanced training and experience in neuropsychology. Bachelor's level Psychometricians assist with testing. Neuropsychologists are assigned patient cases depending on availability, expertise, and interest in a particular disorder. The Attending Neuropsychologist conducts the clinical interview with the patient and if necessary, family members. The Neuropsychologist administers tests, interprets the results and generates a report. A Psychometrician may administer some tests under the supervision of the Neuropsychologist. Patients are usually tested in one day. Written and verbal feedback is tailored to the needs of the patient and referral source. If requested, preliminary verbal feedback can be given to the referral source soon after the evaluation is completed. A written report is generated and follows within two weeks. It is customary to meet with the patient to provide feedback about test results.

Guidelines for Psychiatric Emergencies/ Patients

For Psychiatric Emergencies: (have patient evaluated same day because of possible suicidality, psychosis, or grave disablity) I. Page Psychiatric Consult & Liason Services (4,) 5894 2. If imminent danger of hurting self or others, call security (a) 3-7222

G2/1I2 patients: 1. Call resident and get referral question/ brief hx as well as date patient needs to be seen, tentative discharge date. See asap as early We possible/likely. 2. Review chart. 3. Do an interview, don't rely on resident for full info. Call family or collaterals if questions. 4. For best availability, tell patient's nurse time you want to see him/her. 5. Do chart note for every day seen. If say you're coming back, do. List tests given. 6. Give verbal feedback to resident as well as written. Coordinate with resident regarding feedback to patient/family.

Making referrals to psychiatry: I. Pt can call 498-9111 to schedule an appointment. 2. Neuropsychologist call 498-9111 and give the following info: a) name of patient b) d i a g n o s i s c) what you think they need; ie. type of clinic or medical evaluation d) fax copy of report to 498-4960

Enclosure A

Stanford Comprehensive Movement Disorders Center

Comprehensive Movement Disorders Evaluation Description of Clinical Tests
1. Comprehensive Neurological Consultation (CPT 99245) 2 . Clinical Manual Testing (CPT Code 95834): UPDRS-Unified Parkinson's Disease Rating Scale: is a series of questions and clinical tests to evaluate specific abnormalities of cognitive and motor function and of activities of daily living. Hoehn and Yahr Stage: a clinical score of the overall disease severity Schwab and England Independence Score: a series of questions to determine the patient's

independence status.
Dyskinesia Rating Scale : a clinical score of the intensity and duration of dyskinesias (involuntary

movements).
Fahn-Marsden Dystonia Rating Scale: a clinical score of severity and location of dystonia. 3 . Quantitative Digitography (CPT Code 95999-26-59, 50): computerized objective measures of

movement velocity, speed of movement and timing using a computerized keyboard. In addition temporal abnormalities of movement such as freezing and fatigue are measured and quantified. The measures are sensitive to the OFF versus ON medication state and give an accurate dose responsivity profile, which is the best predictor of outcome of surgery.
4 . Quantitative Range of Motion Analysis (CPT Code 95852-26-59, 50): objective measurements of

the angle, angular velocity and frequency of repetitive pronation/supination are correlated with the patient's rigidity and can be quantified and followed over time under therapeutic interventions (MOTUS Bioengineering, Inc.). Performing the test over 10-20 seconds also yields a measurement of fatigue.
5 . Tremorography (CPT Code 95999-26-59, 50): measurement of the rate, amplitude and frequency

of tremor using a gyroscopic sensor sensitive to angular velocity (MOTUS Bioengineering, Inc.) on various parts of the body involved in tremor. These measurements can also display the temporal change of frequency over time and are sensitive to medication and to surgical interventions.
6 . Computerized Balance Analysis (CPT Code 95999-26-59): balance tests using the Smart Equitest

system that determine which specific components of balance are damaged in Parkinson's disease and predict those that will be responsive to medication and/or surgery.
7 . Gait Analysis, Stand-Walk-Sit Timed Testing (CPT Code 97750-22-99): timed measurements of

reaction time and movement time and of walking a certain distance over several trials.
8 . Neuropsychological Battery (CPT Code

96117): See battery in Enclosure

B.

9 . NIRI (C PT C ode 70551): Scans of brain.

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS

STANFORD UNIVERSITY HOSPITAL SEDATION POLICY AND PROCEDURE I POLICY Medications shall be administered in the Neurodiagnostic Labs as an aide to inducing sleep for EEG recordings and general muscle relaxation for Somatosensory Evoked Potentials without producing the loss of the gag reflex and/or respiratory depression. II PURPOSE The purpose of this policy is to provide a safe means of administering mild sedation for studies performed in the Neurodiagnostic labs. This policy allows physicians to provide their patients with the benefits of sedation/analgesia while minimizing the associated risks.

A need exists to induce sleep in adult patients for EEG recordings when sleep cannot be obtained naturally. The diagnostic value of EEG recordings for certain disorders can be enhanced by recording with the patient asleep. In addition sedation can be used to obtain EEG recordings in patients who may not be able to cooperate on their own. The recording of Somatosensory Evoked Potentials requires that the patient be relaxed without muscle tension. The potentials that are recorded are extremely small in amplitude and requires that a number be averaged together for the measurement. Any muscle tension obscures the EP and can distort it or make it impossible to record. In addition the small electrical stimulus can be unpleasant to some patients causing them to become tense. The use of mild sedation to relax patients increases the yield of the testing in producing interpretable waveforms.
III MEDICATIONS The following medications will be used for sedation in the Neurodiagnostic labs:

A. Chloral Hydrate Use: Induce sleep for EEG recordings Dosage: 50-75 mg/kg Maximum dose: 2000mg Achieve therapeutic levels: 20-40 min. Expected duration of action: 4-8 hr.

3/98

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS

STANFORD UNIVERSITY HOSPITAL SEDATION POLICY AND PROCEDURE B. Diazepam (Valium) Use: Produce muscle relaxation for recording of SSEPs Dosage: 0.2-0.3 mg/kg Maximum dose: 10 mg Achieve therapeutic levels: 45-60 min. Expected duration of action: 6-8 hr.

IV IMPLEMENTATION A. PRE-ADMINISTRATION OF MEDICATION 1. A sedation order should be obtained from the physician ordering the EEG study. This physician should assess the patient's appropriateness for sedation. Assessment should include: history of adverse reaction to anesthesia or sedative medications - airway problems - any current acute or chronic medical problems any history of apnea - current medications - any recent doses of sedative or narcotic medications 2. If an out-patient, instruct patient of the requirement that the patient must have a ride home after the procedure and must be accompanied by a responsible adult. B. ADMINISTRATION OF MEDICATION 1. Technologist or physician will interview patient about their medication history including drug allergies and prior reaction to sedative medications. 2. Medication is to be administered by a physician or nurse as ordered by the referring physician or the Medical Director of the EEG laboratory. The ordering physician and the medical director of the laboratory bear the ultimate responsibility for the safe administration of medication.

3/98

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS

STANFORD UNIVERSITY HOSPITAL SEDATION POLICY AND PROCEDURE I POLICY Medications shall be administered in the Neurodiagnostic Labs as an aide to inducing sleep for EEG recordings without producing the loss of the gag reflex and/or respiratory depression. II PURPOSE The purpose of this policy is to provide a safe means of inducing sleep in adult patients for EEG recordings when sleep cannot be obtained naturally. The diagnostic value of EEG recordings for certain disorders can be enhanced by recording with the patient asleep. In addition sedation can be used to obtain recordings in patient who may not be able to cooperate on their own. This policy allows physicians to provide their patients with the benefits of sedation/analgesia while minimizing the associated risks.

HI MEDICATIONS The following medications will be used for sedation in the Neurodiagnostic labs: A. Chloral Hydrate Dosage: 50-75 mg/kg Maximum dose: 2000mg Achieve therapeutic levels: 20-40 mins Expected duration of action: 4-8 hrs
IV IMPLEMENTATION A. PRE ADMINISTRATION OF MEDICATION 1. A sedation order should be obtained from the physician ordering the EEG study. This physician should assess the patient's appropriateness for sedation. Assessment should include: - history of adverse reaction to anesthesia or sedative medications - airway problems - any current acute or chronic medical problems - any history of apnea - current medications - any recent doses of sedative or narcotic medications

3/98

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS

STANFORD UNIVERSITY HOSPITAL SEDATION POLICY AND PROCEDURE 2. If an out-patient, instruct patient of the requirement that the patient must have a ride home after the procedure and must be accompanied by a responsible adult. B. ADMINISTRATION OF MEDICATION 1. Technologist will interview patient about their medication history including drug allergies and prior reaction to sedative medications. 2. Medication is to be administered by a Registered END Technologist as ordered by the referring physician or the Medical Director of the EEG laboratory. The administering technologist should be under direct supervision of a licensed physician. The ordering physician and the medical director of the laboratory bear the ultimate responsibility of the safe administration of medication by the technical staff. C. DURING PROCEDURE 1. Continually assess and monitor the patient during the administration of sedation. 2. Run continuous EKG as a tracing on the EEG record. 3. Continually assess patient respirations during the EEG recording. 4. Record patient name, dosage, and administrator on drug record. D. POST PROCEDURE 1. Continue to observe the patient until: -they are easily aroused or is at pre-procedure baseline level of consciousness. -patient is able to walk with minimum assistance. 2. Insure the patient has transportation home with a responsible adult.

3/98

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS

STANFORD UNIVERSITY HOSPITAL SEDATION POLICY AND PROCEDURE C. DURING PROCEDURE 1. Continually assess and monitor the patient during the administration of sedation 2. Run continuous EKG as a tracing on the EEG record. 3. Continually assess patient respirations during the EEG/EP recording. 4. Record patient name, dosage, and administrator on drug record. D. POST PROCEDURE 1. Continue to observe the patient until: -they are easily aroused or is at pre-procedure baseline level of consciousness. -patient is able to walk with minimum assistance. 2. Insure the patient has transportation home with a responsible adult.

3/98

DRUG INFORMATION HANDBOOK Generated by CRL TM

Chloral Hydrate
Pronunciation (KLOR al HYE drate) Brand Names Aquachloraie Supprettes Canadian/Mexican Brand Names Novo-Chlorhydrate (Canada); PMS-Chloral Hydrate (Canada) Synonyms Chlorat Hydrated Chloral; Trichloroacetaldehyde Monohydrate Therapeutic Category Hypnotic Sedative Use Short-term sedative and hypnotic (<2 weeks), sedative/hypnotic for dental and diagnostic procedures; sedative prior to EEG evaluations Restrictions C-IV Pregnancy Risk Factor C Contraindications Hypersensitivity to chloral hydrate or any component; hepatic or renal impairment; gastritis or ulcers; severe cardiac disease Warnings/Precautions Use with caution in patients with porphyria; use with caution in neonates, drug may accumulate with repeated use, prolonged use in neonates associated with hyperbilirubinemia; tolerance to hypnotic effect develops, therefore, not recommended for use >2 weeks; taper dosage to avoid withdrawal with prolonged use; trichloroethanol (TCE), a metabolite of chloral hydrate, is a carcinogen in mice; there is no data in humans. Chloral hydrate is considered a second line hypnotic agent in the elderly. Recent interpretive guidelines from the Health Care Financing Administration (HCFA) discourage the use of chloral hydrate in residents of long-term care facilities. Adverse Reactions >10%: Gastrointestinal: Gastric irritation, nausea, vomiting, diarrhea 1% to 10%: Central nervous system: Ataxia, hallucinations, drowsiness, "hangover" effect Dermatologic: Rash, urticaria <1%: Central nervous system: Disorientation, sedation, ataxia, excitement (paradoxical), dizziness, fever, headache, confusion Gastrointestinal: Gastric irritation, flatulence Hematologic: Leukopenia, eosinophilia Miscellaneous: Physical and psychological dependence may occur with prolonged use of large doses Overdosage/Toxicology Symptoms of overdose include hypotension, respiratory depression, coma, hypothermia, cardiac arrhythmias Treatment is supportive and symptomatic; lidocaine or propranolol may be used for ventricular dysrhythmias, while isoproterenol or atropine may be required for torsade de pointes; activated charcoal may prevent drug absorption Drug Interactions Increased toxicity: May potentiate effects of warfarin, central nervous system depressants, alcohol; vasodilation reaction (flushing, tachycardia, etc) may occur with concurrent use of alcohol; concomitant use of furosemide (IM.) may result in flushing, diaphoresis, and blood pressure changes Stability Sensitive to light; exposure to air causes volatilization; store in light-resistant, airtight container Mechanism of Action Central nervous system depressant effects are due to its active metabolite trichloroethanol, mechanism unknown Pharmacodynamics/Kinetics

Page 1

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DRUG INFORMATION HANDBOOK Generated by CRLTI"'

Peak effect: Within 0.5-1 hour Duration: 4-8 hours Absorption: Oral, rectal: Well absorbed Distribution: Crosses the placenta; negligible amounts appear in breast milk Metabolism: Rapidly to trichloroethanol (active metabolite); variable amounts metabolized in liver and kidney to trichloroacetic acid (inactive) Half-life: Active metabolite: 8-11 hours Elimination: Metabolites excreted in urine, small amounts excreted in feces via bile Usual Dosage Children: Sedation, anxiety: Oral, rectal: 5-15 mg/kg/dose every 8 hours, maximum: 500 mg/dose Prior to EEG: Oral, rectal: 20-25 mg/kg/dose, 30-60 minutes prior to EEG; may repeat in 30 minutes to maximum of 100 mg/kg or 2 g total Hypnotic: Oral, rectal: 20-40 mg/kg/dose up to a maximum of 50 mg/kg/24 hours or 1 g/dose or 2 g/24 hours Sedation, nonpainful procedure: Oral: 50-75 mg/kg/dose 30-60 minutes prior to procedure; may repeat 30 minutes after initial dose if needed, to a total maximum dose of 120 mg/kg or 1 g total Adults: Oral, rectal: Sedation, anxiety: 250 mg 3 times/day Hypnotic: 500-1000 mg at bedtime or 30 minutes prior to procedure, not to exceed 2 g/24 hours Dosing adjustment/comments in renal impairment: Cl, <50 mUminute: Avoid use Hemodialysis: Dialyzable (50% to 100%); supplemental dose is not necessary Dosing adjustment/comments in hepatic impairment: Avoid use in patients with severe hepatic impairment Dietary Considerations Alcohol: Additive CNS effects, avoid use Administration Do not crush capsule, contains drug in liquid form Monitoring Parameters Vital signs, 02 saturation and blood pressure with doses used for conscious sedation Test Interactions False-positive urine glucose using Clinitest method; may interfere with fluorometric urine catecholamine and urinary 17-hydroxycorticosteroid tests Patient Information Take a capsule with a full glass of water or fruit juice; swallow capsules whole, do not chew; avoid alcohol and other CNS depressants; avoid activities needing good psychomotor coordination until CNS effects are known; drug may cause physical or psychological dependence; avoid abrupt discontinuation after prolonged use; if taking at home prior to a diagnostic procedure, have someone else transport Nursing Implications Gastric irritation may be minimized by diluting dose in water or other oral liquid Dosage Forms Capsule: 250 mg, 500 mg Suppository, rectal: 324 mg, 500 mg, 648 mg Syrup: 250 mg/5 mL (10 mL); 500 mg/5 mL (5 mL, 10 mL, 480 mL) References American Academy of Pediatrics, Committee on Drugs and Committee on Environmental Health," Use of Chloral Hydrate for Sedation in Children," Pediatrics, 1993, 92(3):471-3. Buck ML, "Chloral Hydrate Use During Infancy,"Neonatal Pharmacology Quarterly, 1992, 1(1):31-7. Buur T, Larsson R, and Norlander B, "Pharmacokinetics of Chloral Hydrate Poisoning Treated With Hemodialysis and Hemoperfusion,"Ada Med Scand, 1988, 223(3):269-74. Donovan KL and Fisher DJ, "Reversal of Chloral Hydrate Overdose With Flumazenil," Br Med J (Clio Res Ed), 1989, 298(6682):1253.

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DRUG INFORMATION HANDBOOK Generated by CRL TM

Kauffman RE, "Chloral Hydrate - Is It a Carcinogenic Hazard?,"Pedialr Alert, 1991, 16(6) 21-22. Laptook AR and Rosenfeld CR, "Chloral Hydrate Toxicity In a Preterm Infant," Pediatr Pharmacol New York, 1984, 4(3):161-5. Mayers DJ, Hindmarsh KW, Gorecki DK, et al, "Sedative/Hypnotic Effects of Chloral Hydrate in the Neonate: Trichloroethanol or Parent Drug?" Dev Pharmacol mar, 1992, 19(2-3):141-6. Mayers DJ, Hindmarsh KW, Sankaran K, et al, "Chloral Hydrate Disposition Following Single-Dose Administration to Critically III Neonates and Children,"Dev Pharmacol Ther, 1991, 16(2):71-7. Meyer E, Van Bocxlaer JF, Lambert WE, et al, "Determination of Chloral Hydrate and Metabolites in a Fatal Intoxication,"J Ana/ Toxicol, 1995, 19(2):124-6. Mowry JB, Wilson GA, and Schreiner R, "Effect of Exchange Transfusion in Chloral Hydrate Overdose," Vet Hum Toxicol, 1983, 25:15-21. Salmon AG, Kizer KW, Zeise L, et al, "Potential Carcinogenicity of Chloral Hydrate - A Review," J Toxicol Clin Toxicol, 1995, 33(2):115-21. Seger D and Schwartz G, "Chloral Hydrate: A Dangerous Sedative for Overdose Patients? Pediatr Emerg Care, 1994, 10(6):349-50. Sing K, Erickson T, Amitai Y, et al, "Case Series of Chloral Hydrate Toxicity From Oral and Intravenous Administration," Vet Hum Toxicol, 1993, 35:339. Steinberg AD, "Should Chloral Hydrate be Banned? Pediatrics, 1993, 92(3)442-6. Zeltzer LK, Altman A, Cohen D, et al, "American Academy of Pediatrics Report of the Subcommittee on the Management of Pain Associated With Procedures in Children Wdh Cancer," Pediatrics, 1990, 86(5 Pt 2):826-31.

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DRUG INFORMATION HANDBOOK Generated by CRL TM

Diazepam
Pronunciation (dye AZ e pam) Related Information Adult ACLS Algorithm, Electrical Conversion Anticonvulsants by Seizure Type Benzodiazepines Comparison Convulsive Status Epilepticus Febrile Seizures Brand Names Dizac Injection; Valium Canadian/Mexican Brand Names Apo-Diazepam (Canada); Diazemuls (Canada); E Pam (Canada); Meval (Canada); Novo-Dipam (Canada); PMS-Diazepam (Canada); Vivol (Canada) Therapeutic Category Antianxiety Agent Anticonvulsant Benzodiazepine Sedative Use Management of general anxiety disorders, panic disorders, and provide preoperative sedation, light anesthesia, and amnesia; treatment of status epilepticus, alcohol withdrawal symptoms; used as a skeletal muscle relaxant Restrictions C-IV Pregnancy Risk Factor D Pregnancy/Breast Feeding Implications Clinical effects on the fetus: Crosses the placenta. Oral clefts reported, however, more recent data does not support an association between drug and oral clefts; inguinal hernia, cardiac defects, spina bifida, dysmorphic facial features, skeletal defects, multiple other malformations reported; hypotonia and withdrawal symptoms reported following use near time of delivery Breast-feeding/lactation: Crosses into breast milk Clinical effects on the infant: Sedation; American Academy of Pediatrics reports that USE MAY BE OF CONCERN. Contraindications Hypersensitivity to diazepam or any component; there may be a cross-sensitivity with other benzodiazepines; do not use in a comatose patient, in those with pre-existing CNS depression, respiratory depression, narrow-angle glaucoma, or severe uncontrolled pain; do not use in pregnant women Warnings/Precautions Use with caution in patients receiving other CNS depressants, patients with low albumin, hepatic dysfunction, and in the elderly and young infants. Due to its long-acting metabolite, diazepam is not considered a drug of choice in the elderly; long-acting benzodiazepines have been associated with falls in the elderly. Adverse Reactions >10%: Cardiovascular: Cardiac arrest, hypotension, bradycardia, cardiovascular collapse, tachycardia, chest pain Central nervous system: Drowsiness, ataxia, amnesia, slurred speech, paradoxical excitement or rage, fatigue, lightheadedness, insomnia, memory impairment, headache, anxiety, depression Dermatologic: Rash Endocrine & metabolic: Decreased libido Gastrointestinal: Xerostomia, changes in salivation, constipation, nausea, vomiting, diarrhea, increased or

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decreased appetite Local: Phlebitis, pain with injection Neuromuscular & skeletal: Dysarthria Ocular: Blurred vision, diplopia Respiratory: Decrease in respiratory rate, apnea, laryngospasm Miscellaneous: Diaphoresis 1% to 10%: Cardiovascular: Syncope, hypotension Central nervous system: Confusion, nervousness, dizziness, akathisia Dermatologic: Dermatitis Gastrointestinal: Weight gain or loss Neuromuscular & skeletal: Rigidity, tremor, muscle cramps Otic: Tinnitus Respiratory: Nasal congestion, hyperventilation Miscellaneous: Hiccups <1%: Endocrine & metabolic: Menstrual irregularities Hematologic: Blood dyscrasias Neuromuscular & skeletal: Reflex slowing Miscellaneous: Physical and psychological dependence with prolonged use Overdosage/Toxicology Symptoms of overdose include somnolence, confusion, coma, hypoactive reflexes, dyspnea, hypotension, slurred speech, impaired coordination Treatment for benzodiazepine overdose is supportive. Rarely is mechanical ventilation required. Flumazenil has been shown to selectively block the binding of benzodiazepines to CNS receptors, resulting in a reversal of benzodiazepine-induced CNS depression, but not respiratory depression Drug Interactions Diazepam and desmethyldiazepam are cytochrome P-450 2C enzyme substrates Decreased effect: Enzyme inducers may increase the metabolism of diazepam Increased toxicity: CNS depressants (alcohol, barbiturates, opioids) may enhance sedation and respiratory depression; cimetidine may decrease the metabolism of diazepam; cisapride can significantly increase diazepam levels; valproic acid may displace diazepam from binding sites which may result in an increase in sedative effects; selective serotonin reuptake inhibitors (eg, fluoxetine, sertraline, paroxetine) have greatly increased diazepam levels by altering its clearance Stability Protect parenteral dosage form from light; potency is retained for up to 3 months when kept at room temperature; most stable at pH 4-8, hydrolysis occurs at pH <3; do not mix I.V. product with other medications Mechanism of Action Depresses all levels of the CNS, including the limbic and reticular formation, probably through the increased action of gamma-aminobutyric acid (GABA), which is a major inhibitory neurotransmitter in the brain Pharmacodynamics/Kinetics I.V. for status epilepticus: Onset of action: Almost immediate Duration: Short, 20-30 minutes Absorption: Oral: 85% to 100%, more reliable than I.M. Protein binding: 98% Metabolism: In the liver Half-life:

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Parent drug: Adults: 20-50 hours, increased half-life in neonates, elderly,.and those with severe hepatic disorders Active major metabolite (desmethyldiazepam): 50-100 hours, can be prolonged in neonates Usual Dosage Oral absorption is more reliable than I.M. Children: Conscious sedation for procedures: Oral: 0.2-0.3 mg/kg (maximum: 10 mg) 45-60 minutes prior to procedure Sedation or muscle relaxation or anxiety: Oral: 0.12-0.8 mg/kg/day in divided doses every 6-8 hours I.M., I.V.: 0.04-0.3 mg/kg/dose every 2-4 hours to a maximum of 0.6 mg/kg within an 8-hour period if needed Status epilepticus: Infants 30 days to 5 years: I.V.: 0.05-0.3 mg/kg/dose given over 2-3 minutes, every 15-30 minutes to a maximum total dose of 5 mg; repeat in 2-4 hours as needed or 0.2-0.5 mg/dose every 2-5 minutes to a maximum total dose of 5 mg >5 years: IV.: 0.05-0.3 mg/kg/dose given over 2-3 minutes every 15-30 minutes to a maximum total dose of 10 mg, repeat in 2-4 hours as needed or 1 mg/dose given over 2-3 minutes, every 2-5 minutes to a maximum total dose of 10 mg Rectal: 0.5 mg/kg, then 0.25 mg/kg in 10 minutes if needed Adolescents: Conscious sedation for procedures: Oral: 10 mg I.V.: 5 mg, may repeat with 1/2 dose if needed Adults: Anxiety/sedation/skeletal muscle relaxation: Oral: 2-10 mg 2-4 times/day I.M., I.V.: 2-10 mg, may repeat in 3-4 hours if needed Status epilepticus: I.V.: 5-10 mg every 10-20 minutes, up to 30 mg in an 8-hour period; may repeat in 2-4 hours if necessary Elderly: Oral: Initial: Anxiety: 1-2 mg 1-2 times/day; increase gradually as needed, rarely need to use >10 mg/day Skeletal muscle relaxant: 2-5 mg 2-4 times/day Hemodialysis: Not dialyzable (0% to 5%); supplemental dose is not necessary Dosing adjustment in hepatic impairment: Reduce dose by 50% in cirrhosis and avoid in severe/acute liver disease Dietary Considerations Alcohol: Additive CNS depression has been reported with benzodiazepines; avoid or limit alcohol Administration In children, do not exceed 1-2 mg/minute IVP; adults 5 mg/minute Monitoring Parameters Respiratory rate, heart rate, blood pressure with I.V. use Reference Range Therapeutic: Diazepam: 0.2-1.5 jc/mL (SI: 0.7-5.3 lanol/L); N-desmethyldiazepam (nordiazepam): 0.1-0.51.1g/mL (SI: 0.35-1.8 nmol/L) Test Interactions False-negative urinary glucose determinations when using Clinisttio1D or Diastix Patient Information Avoid alcohol and other CNS depressants; avoid activities needing good psychomotor coordination until CNS effects are known; drug may cause physical or psychological dependence; avoid abrupt

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discontinuation after prolonged use Nursing Implications Provide safety measures (ie, side rails, night light, and call button); supervise ambulation Dosage Forms Injection: 5 mg/mL (1 mL, 2 mL, 5 mL, 10 mL) Injection, emulsified (Dizac): 5 mg/mL (3 mL) Solution, oral (wintergreen-spice flavor): 5 mg/5 mL (5 mL, 10 mL, 500 mL) Solution, oral concentrate: 5 mg/mL (30 mL) Tablet: 2 mg, 5 mg, 10 mg References Allikmets E, et al, "Long-term Use of Benzodiazepines: Abrupt Withdrawal Versus Withdrawal Under Nifedipine Cover," Pharmacol Toxicol, 1995, 76(Suppl 3):Abstr 8. Klotz U, Avant GR, Hoyumpa A, et al, "The Effects of Age and Liver Disease on the Disposition and Elimination of Diazepam in Adult Man,"J Clin Invest, 1975, 55(2):347-59. Pornara N, Stanley B, Block R, et al, "Increased Sensitivity of the Elderly to the Central Depressant Effects of Diazepam,"J Clin Psychiatry, 1985, 46(5):185-7. Reidenberg MM, Levy M, Warner H, et al, "Relationship Between Diazepam Dose, Plasma Level, Age, and Central Nervous System Depression," Clin Pharmacol Trier, 1978, 23(4):371-4. Rosman NP, Colton T, Labazzo J, et al, "A Controlled Trial of Diazepam Administered During Febrile Illnesses to Prevent Recurrence of Febrile Seizures," N Eng! J Med, 1993, 329(2):79-84. Traeger SM and Haug MT 3d, "Reduction of Diazepam Serum Half-Life and Reversal of Coma by Activated Charcoal in a Patient With Severe Liver Disease: J Toxicol Clin ToxicoI 1986, 24(4):329-37. Votey SR, Bosse GM, Bayer MJ, et al, "Flumazenil: A New Benzodiazepine Antagonist," Ann Emerg Med, 1991, 20(2):181-8. Zeltzer LK, Altman A, Cohen D, et al, "Report of the Subcommittee on the Management of Pain Associated With Procedures in Children With Cancer," Pediatrics, 1990, 86(5 Pt 2):826-31.

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ANESTHESIOLOGY AND CRITICAL DRUG HANDBOOK Generated by CRLTM

CONSCIOUS SEDATION
Note that conscious sedation may only be administered by those specifically trained and approved by Stanford Hospital to do so.
The goal of conscious sedation is to produce a state where: 1) patients are able to tolerate unpleasant procedures; 2) adequate cardiorespiratory function is maintained; and 3) patients are able to respond purposefully to verbal commands and/or tactile stimulation. The American Society of Anesthesiologists Task Force on Sedation and Analgesia by Non-Anesthesiologists has recommended that the term "conscious sedation" be replaced with" sedation and analgesia" as this more accurately describes the therapeutic goal desired. When administered appropriately, sedation/analgesia should result in a patient who is lightly sedated, cooperative on demand, amnesic, and free from pain and anxiety.

PATIENT EVALUATION
A patient history, physical examination (including height, weight, assessment of airway patency, auscultation of the lungs and heart), and laboratory evaluation (based on patient's underlying medical condition) should be performed. The patient's medical history should include: 1. All current medications and drug allergies 2. Previous adverse effects to sedation/analgesia 3. Time/nature of last oral intake (clear liquids >2-3 hours, solids >6-8 hours) 4. History of alcohol, tobacco, illicit drug use 5. Any abnormalities of major organ function A thorough medication history is important to prevent potential drug interactions. For example, meperidine is contraindicated in a patient taking a monoamine oxidase inhibitor (MAGI). It is recommended that the MAGI be discontinued two weeks prior to the anticipated administration of meperidine Opioids and CNS depressants can increase the potential for apnea and oversedation when administered with a benzodiazepine. The clearance of diazepam , but not midazolam, is decreased and its half-life increased with cimetidine . Indinavir and saquinavir may inhibit the metabolism of midazolam and increase the potential for prolonged sedation. Ritonavir can greatly increase the plasma concentration of midazolam, diazepam, and meperidine; these agents should not be used in a patient taking ritonavir.

PATIENT COUNSELING
Patients should be informed of the risks, benefits, and limitations of sedation/analgesia and of potential alternatives.

MONITORING
The following data should be recorded starting before the procedure and continued through the recovery period: 1. Drugs administered (drug, route, site, time, dose) 2. Oxygen saturation (via pulse oximetry) 3. Response to verbal commands (when appropriate) 4. Pulmonary ventilation (through observation of spontaneous respiratory activity or auscultation of breath sounds) 5. Blood pressure and heart rate 6. EKG (for patients with significant cardiovascular disease) Minimally, the patients hemodynamic variables, ventilatory status, and oxygenation status should be recorded before the beginning of the procedure, after administration of sedative/analgesic agents, at completion of the procedure, during initial recovery, and at discharge. However, these variables are normally recorded at regular intervals (eg, every 5 minutes) during the procedure. The frequency of vital signs monitoring may need to be individualized on a case-to-case basis. Patients who are chronically or acutely ill or debilitated, or those who deteriorate during the diagnostic or therapeutic procedure may require more frequent measurements of vital signs. The conduct of the procedure may practically preclude monitoring/recording of a given vital sign at a routine interval. Signs and symptoms of toxicity associated with sedation/analgesia include deep sedation, somnolence, confusion,

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respiratory depression, apnea, respiratory arrest, hypotension, cardiac arrest, nausea and vomiting, diminished reflexes, impaired coordination, and severe changes in vital signs. It is critical that an appropriately trained individual other than the person performing the procedure be present to continuously monitor the patient throughout the procedure and recovery.

EQUIPMENT REQUIREMENTS
The following equipment and supplies should be present or readily available. 1. Oxygen source; supplemental oxygen should be administered when clinically indicated (eg, hypoxemia) 2. Suction 3. Appropriately sized airway equipment and means of positive-pressure ventilation 4. Emergency resuscitation drugs 5. Pharmacologic antagonists (e.g., naloxone for opioids, flumazenil for benzodiazepines) 6. Intravenous equipment; for patients receiving drugs intravenously, I.V. access should be maintained throughout the whole procedure and until the patient is not at risk for serious adverse events from the drugs administered (e.g., cardiorespiratory depression).

AGENT SELECTION/DOSE TITRATION

Sedatives (eg, midazolam , diazepam , chloral hydrate, droperidol ) are routinely used to decrease anxiety and promote somnolence. Analgesics (eg, morphine , meperidine fentanyl ) are routinely used to relieve pain. Combinations of opioids and sedatives may increase the incidence of adverse effects. When used together, each agent should be administered individually in order to allow the desired effect of each agent to be achieved. When given intravenously, sedative/analgesic drugs should be administered in small, incremental doses until the desired effect is achieved (titrate to effect). Please refer to the individual drug monographs for appropriate dosing guidelines. Care must be taken to allow a sufficient time between doses to allow the effect of each dose to be seen. Dosage reductions may be required in the chronically ill or elderly as well as with the concomitant administration of an opioid and sedative agent (e.g., benzodiazepine). Additional time should be allowed between doses when drugs are administered by nonintravenous routes (e.g., oral, rectal, I.M.) secondary to the time required for drug absorption.

RECOVERY

Patients may continue to be at risk for complications after the procedure and must be monitored (level of consciousness, vital signs, respiratory function) throughout the recovery period until meeting discharge criteria. If a reversal agent has been administered, an appropriate time (up to 2 hours) should have elapsed to ensure that resedation does not occur secondary to the agents short duration of action when compared to the sedation/analgesia agents. Patients must be discharged with an accompanying responsible adult. The patient and accompanying adult should be advised (both verbally and in writing) regarding any limitations on the patients activity (eg, do not operate machinery or drive an automobile for 24 hours), diet, and medication use. In addition, the patient should be given a 24-hour emergency contact telephone number in case problems arise.

REFERENCES AND RECOMMENDED READING "Practice Guidelines for Sedation and Analgesia by Non-Anesthesiologists. A Report by the American Society of Anesthesiologist Task Force on Sedation and Analgesia by Nonanesthesiologists Anesthesiology, 1996, 84(2):459-71. Holland CA, "Conscious Sedation Policy Development and Review,"AANA J, 1995, 63(3):196-7. Holzman RS, Cullen DJ, Eichhorn JH, et al, "Guidelines for Sedation by Nonanesthesiologists During Diagnostic and Therapeutic Procedures. The Risk Management Committee of the Department of Anesthesia of Harvard Medical School," J Clin Anesth, 1994, 6(4):265-76. Kaplan RF, "Sedation and Analgesia in Pediatric Patients for Procedures Outside the Operating Room," Paper presented at the ASA 1996 Annual Refresher Course Lectures, New Orleans, LA, 1996 Oct 23. Krikorian SA, "Intravenous Conscious Sedation," US Pharmacist, 1997, HS26-36. Malviya S and Voepel-Lewis T, "Sedation of Children Outside the Operating Room," Progress in Anesthesiology, 1995, 9:399-411.

PATIENT INFORMATION: VALIUM PREMEDICATION FOR SOMATOSENSORY EVOKED POTENTIALS Your doctor has ordered an electrical test of your body's ability to transmit sensory information from your hands or feet to your brain. Because muscle tightness in the neck and back interferes with the recording of these impulses, your doctor has indicated that you can be given a small dose of Valium (diazepam) to relax these muscles. Since Valium may occasionally cause sleepiness, which lasts longer than the time required for the test, it will be necessary for you to have someone with you who can assist you after the test. You should not operate a motor vehicle or dangerous machinery for a period of six hours after receiving the Valium. Please advise if any of the following situations applies to you: 1. 2. 3. 4. You are pregnant or suspect you might be. You have any known allergy to Valium or have had any adverse reaction to it. You do not wish to receive Valium. You are not accompanied by anyone who can assist you if you are sleepy at the end of the test.

I have read and understand these instructions prior to receiving Valium, 10 mg, p.o.

Date

Signature of Parent

STANFORD HOSPITAL & CLINICS

Stanford University Medical Center

Laboratory 300 Pasteur Drive, Room 1131 Stanford, CA 94305 (650) 723-7181

EEG INSTRUCTIONS
An appointment has been made for to have an electroencephalogram (EEG) test in the EEG Laboratory at Stanford Hospital. You have been scheduled for the following: Date: Time: [ ] Routine EEG Sleep EEG [ ] Sleep-deprived EEG [ ] Video EEG___ hours

It is important for you to be on time. If you are late, it may be necessary to reschedule your EEG. The above time has been reserved for you. If you do not intend to use this time, please notify us so that we can offer the appointment to someone else. Plan to arrive 30 minutes early to register at the Admitting Desk in the main hospital lobby. They will provide you will labels, which you will need to bring with you to your appointment. Directions in the hospital: Take escalators/elevators next to gift shop to third floor. Turn left off the escalators/elevators and then the first right. Follow signs to EEG lab. The test takes approximately one to one-and-a-half hours (except video EEG) and is entirely painless. In preparation for the examination you should plan the following: 1. Wash and dry your hair thoroughly. Your scalp should be clean and free of oils, conditioners, hairsprays, etc. 2. Eat a meal (or at least a snack) before the EEG to help stabilize your blood sugar level. 3. If you take any medications, continue to take them as directed by your doctor. 4. Dress comfortably. If you have been scheduled for a sleep EEG or a sleep deprived EEG, we will want you to fall asleep in our lab. Please note the following instructions in addition to those listed above: 1. Arrange to have someone else drive you home after the EEG. We may wish to give you a mild sedative to help you fall asleep in the lab. The medication we use is chloral hydrate. Please let the technologist know if you are allergic to this medication. 2. Avoid caffeine beverages/foods (e.g., coffee, tea, colas, chocolate, etc.) and alcohol after midnight before the test. 3. If you have been scheduled for a sleep-deprived EEG, sleep only until midnight prior to the EEG. You should stay awake the remainder of the time until you come in for your EEG. If you have been scheduled for a video EEG, you should bring with you: money to purchase lunch/snacks/drinks or you may bring these items from home with you. You may bring something quiet to work on (e.g., book to read, crossword puzzles, knitting etc.) If you have any questions, please feel free to contact us.

Stanford Health Care 300 Pasteur Drive Stanford, CA 94305 EEG INSTRUCTIONS

EEG Laboratory Room 113132 (650) 723-7181

An appointment has been made for you to have an electroencephalographic (EEG) test in the EEG Laboratory at Stanford Hospital. You have been scheduled for the following: Routine EEG DATE: Sleep EEG Sleep-deprived EEG TIME: It is important for you to be on time. If you are late, it may be necessary to reschedule your EEG. The above time has been reserved for you. If you do not intend to use this time, please notify us so that we can offer the appointment to someone else.
Plan to arrive about 15-20 minutes early so that you can register at the Admitting Desk in the main hospital lobby. They will provide you with labels.

The test takes approximately one to one-and-a-half hours and is entirely painless. In preparation for the examination you should plan the following: I. Wash and dry your hair thoroughly. Your scalp should be clean and free of oils, conditioners, hair sprays, etc. 2. Eat a meal (or at least a snack) before the EEG to help stabilize your blood sugar level. 3. If you take any medications, continue to take them as directed by your doctor. 4. Dress comfortably. If you have been scheduled for a sleep EEG or a sleep-deprived EEG, we will want you to fall asleep in our lab. Please note the following instructions in addition to those listed above: I. Arrange to have someone else drive you home after the EEG. We may wish to give you a mild sedative to help you fall asleep in the laboratory. The medications we use are chloral hydrate. Please let the technologist know if you are allergic to this medication. 2. Avoid caffeine beverages/foods (e.g., coffee, tea, colas, chocolate, etc.) and alcohol after midnight before the test. 3. If you have been scheduled for a sleep-deprived EEG, do not sleep the entire night before the test. You may take an afternoon nap, if you wish, to prepare for staying up all night. If you have any questions, please feel free to contact us.

Rev. 7/2010

STANFORD UNIVERSITY MEDICAL CENTER

EMG LABORATORY
ROOM: 113134 Phone: 650-723-6888
EMG INSTRUCTIONS PLEASE READ CAREFULLY

An appointment has been made for you to have an ELECTROMYOGRAM (EMG) and nerve conduction velocity (NCV) testing in our laboratory. DATE: _________________________ TIME: _________________

Please be on time; if you are [ate, it may be necessary to reschedule your test. In the event you are unable to keep your appointment, please call the lab at least 24 hours before your appointment of cancel at 650-723-6888. Please arrive at least 20 minutes prior to your appointment and stop at registration to pick up labels. Hospital registration is located on the first floor of the hospital. Enter the hospital through the main entrance and turn left to reach registration. To reach the lab take the escalator or elevators located in the corridor by the Gift Shop and proceed to the third floor. On the third floor turn left into the main corridor and follow the overhead signs to the EMG lab. The testing is performed in two parts. The first part is the nerve conduction velocity (NCV) test which evaluates the health of the peripheral nerve by recording how fast an electrical impulse travels through it. This involves electrical stimulation of nerves in the arm and/or leg. The second part is the muscle response test (EMG) which requires the insertion of a tiny needle into different muscles. Nerve and muscle diseases alter the pattern of activity in muscles. The entire test takes approximately 1/2-2 hours. Following the testing, the data acquired will be analyzed and a written report will be prepared and sent to your referring physician. PREPARATIONS: Eat normally, and if you take medications continue to take them as directed by your doctor unless you are specifically requested to do otherwise. Please advise the lab staff is you are diabetic, taking anticoagulants (blood thinning medication, such as. coumadin) or if you have any type of blood disorder which may cause excessive bleeding, such as hemophilia. If you are under treatment for myasthenia gravis, please contact the laboratory forty-eight hours prior to testing for special instructions. Dress comfortably and wear loose clothing that permits easy access to the limbs. If you have any questions. please feel free to contact us.

Stanford University Medical Center 300 Pasteur Drive Stantbrd, CA 94305

EEG Laboratory Room H3132 (650) 723-7181

AMBULATORY EEG INSTRUCTIONS

DATE: TIME: am/pm

Your child's physician has ordered an Ambulatory Electroencephalographic (EEG). This study is done on an outpatient basis. Electrodes are placed on the surface of your child's scalp that will be connected by thin wires that run down from your child's head to a recording unit. You will return home wearing the recorder for 24 hours. It is a noninvasive procedure and you will feel no pain.Please be on time: if you are late, it may be necessary to reschedule your test. In the event you are unable to keep your appointment, please call the lab at least 24 hours prior to your appointment. Plan to arrive 30 minutes early prior to the appointment so that you may register at the Admitting Desk at the Lucile Salter Pachard Children's Hospital in the main lobby. They will provide you with labels. To reach the EEG laboratory at Stanford Hospital, follow the main hallway on the first floor into the Stanford Hospital. Turn left at the Gift Shop and take the escalators to the third floor. When exiting the escalators turn left and then your first right. Please also follow signs that indicate EEG Laboratory. In preparation for the ambulatory EEG you should plan the following: I. Bathe, wash and dry your child's hair thoroughly. Their scalp should be clean and free of oils, conditioners, hair sprays, etc... Your child will be unable to bathe or swim during the 24 hour test period. Water will severely damage the recording unit. 2. Your child must/should wear a shirt that either buttons or zips up the front. A pullover shirt will knock electrodes off or out of their precise position. 3. If your child takes any medications, continue to take them as directed by their doctor. After you leave the hospital: 1. DO NOT let your child bathe, shower or swim. Water will severely damage the recording unit. 2. Try not to alter their daily routine. The electrodes are designed to withstand body perspiration even under strenuous physical activity. The only limitation is that you can not get the recording unit wet. 3. You will be required to keep a detailed diary. Noting the time of the day from the recording unit, write down all activities, symptoms or sensations they experience. Please be as thorough as possible. 4. You will be required to return the following day at approximately the same time. Please see the attached brochure "What you should know about your test" If you have any questions, please feel free to contact us at the number above.

Stanford Hospital and Clinics Infection Control Manual

Section 10.00

INFECTION CONTROL RESPONSIBILITIES FOR EEG/EMG I.

INTRODUCTION
The Stanford Hospital and Clinics (SHC) Infection Control Program is designed to prevent infections in patients and personnel. This document describes the role of EEG/EMG personnel in the implementation of the SHC Infection Control Program. EEG/EMG personnel must comply with infection control policies and procedures to minimize the risk of transmission of nosocomial (hospital and clinic-associated) infections to patients and personnel. The Program incorporates patient infection prevention and control measures as well as systems of barrier precautions, to be used by ALL personnel for contact with blood, moist body substances, and non-intact skin of ALL patients, regardless of the patient's diagnosis. In the implementation of this approach, EEG/EMG personnel must assess the anticipated exposure to blood, body substances, and non-intact skin of any patient. Criteria Based Performance Appraisals include criteria requiring compliance with Infection Control and Epidemiology Department (ICED) policies and procedures. Policies and procedures outlined in this document include those aspects of the SHC Infection Control Program, which are relevant to EEG/EMG personnel. Although much of this information is mentioned in the Infection Control Manual, this overview highlights those areas where EEG/EMG personnel can be most effective in preventing hospital-associated infections.

H. EMPLOYEE REPONSIBILITIES IN INFECTION CONTROL A. Responsibilities: 1. All personnel must comply with ICED policies and procedures to minimize the risk of transmission of nosocomial (hospital-associated) infections to patients and personnel. Perform hand hygiene before and after contact with each patient, before performing each invasive procedure, before contact with food, after contact with patient's body fluids, after removing gloves, after using rest rooms, and before and after contact with eyes, nose or mouth. Consume food or liquid in designated locations away from patient care areas, charting areas, or specimen holding areas to prevent the risk of acquiring gastrointestinal infection caused by microorganisms which may be present in the patient environment. Cover non-intact skin with band-aids or other impermeable covering. Wear gloves for contact or anticipated contact with any patient's body fluids, mucous membranes or non-intact skin, and for handling items moist with body fluids. Remove gloves and perform hand hygiene immediately upon

2.

3.

4. 5.

Stanford Hospital and Clinics infection Control Manual

Section 10.00

6. 7.

8.

9.

completion of each individual procedure requiring gloves. A new pair of gloves must be used for each task on the same patient. DO NOT WEAR GLOVES AWAY FROM PATIENT'S BEDSIDE. Wear a mask and protective eyewear when splatter or aerosolization of blood or body fluids is anticipated. Wear a gown when there is close contact with a patient's non-intact skin and when it is likely that your clothing may become soiled with a patient's body fluids. Do not report to work until symptoms are no longer present if you have draining skin lesions, rash, flu-like symptoms (e.g., sore throat with fever and arthralgia) or an acute diarrhea] illness. Use single dose medication vials, or single use pre-filled syringes to flush IV lines/saline locks, to prevent transmission of microorganisms during re-entry into multi-dose vials. Access multiple dose medication vials using sterile technique. Do not take multi-dose vial into patient room or exam room. Discard vials if contamination has occurred during use of vial(s), or if contents appear cloudy or vial is cracked, and when manufacturers' expiration date on the label has passed. When accessing insulin, use aseptic technique and keep vial refrigerated at the medicine station. Sterile items processed at SHC do not have an expiration date. Sterile items must be inspected by the user before the package is opened. If the package is torn, wet, has a broken seal, or is otherwise damaged it is not to be used. If contaminated item is disposable, it must be removed from use and returned to Materials Management. If contaminated item is reusable, return item to Supply Processing for inspection and reprocessing. Commercially sterilized packages and crash cart modules that contain materials that become outdated (e.g. medication, batteries) are dated with an expiration date. Store refrigerated medications, food products and patient specimens in separate refrigerators. Use safety syringes, needles and other sharps to prevent blood-bome pathogen exposure. Refer to Safety Sharp Devise Use policy in the SHC Safety Manual. Consider all used needles, syringes and sharps (e.g., scalpels) to be contaminated. Dispose of attached needle and syringe in puncture-resistant containers. When the container is three-fourths full, the container should be sealed and replaced with a new one, to prevent injury from needles protruding from a "too-full" container opening. Handle all patient specimens as if they contain biohazardous material, including wearing gloves, and placing specimens in impermeable plastic bags immediately after obtaining specimen. Handle all soiled linen in the same careful manner, including wearing gloves when linen is contaminated with body fluids and placing soiled linen in moisture proof plastic bags. Use disposable electronic thermometer covers for taking temperatures for each patient. Clean electronic thermometer base daily with a hospitalapproved disinfectant wipe.

10.

11. 12.

I3.

14.

15.

16.

Stanford Hospital and Clinics

Infection Control Manual

Section 10.00

17. 18.

19.

20.

21. 22. 23.

24.

Use disposable equipment for one patient only (and for one time only, if so stated by the manufacturer), and then discard in the appropriate receptacle. Place contaminated reusable patient care instruments or equipment in designated containers. Send to Supply Processing for decontamination and reprocessing by trained personnel. Assure that the disposable resuscitation bags with disposable mouthpieces for use during emergency mouth-to-mouth resuscitation are readily available in each patient care area. Personnel are advised to use disposable mouthpieces during resuscitation efforts. Dispose of patient care equipment that contains liquid blood (e.g., pleurovacs, blood administration bags, and tubing containing liquid blood) in waste container labeled "Biohazardous Waste". Instruct patients on infection control concepts, such as the proper use of tissues and appropriate hand washing technique, when indicated. Place patients who soil their environment with moist body substances in private rooms. Review policy 5.10 in the Infection Control Manual for instruction on management of patients with specific diseases requiring precautions or isolation. Contact ICED at extension 5-1106 or pager 1-6167 when a patient is on Respiratory, Droplet or Contact Precautions.

B.

Employee Immunity and Immunizations: 1. Personnel must be vaccinated against or immune to measles and rubella. Personnel should contact Occupational Health Services (OHS) to determine their immunity to chickenpox. Personnel who are not immune to chickenpox and who have household exposure to a person with the infection must contact OHS immediately after such infection is diagnosed in a household member. Immunizations to measles, rubella and chickenpox are provided free of charge through OHS. Personnel who have a household exposure to a communicable disease (e.g. mumps, meningococcal meningitis, tuberculosis, SARS) must contact OHS immediately after such infection is diagnosed in a household member. Personnel who have contact with blood and body fluids should be immunized against hepatitis B virus infection if not already immune, or sign a Vaccination Declination Statement. Personnel may obtain this immunization from OHS.

2.

3.

C.

Post-Exposure Follow-Up For Employees Exposed To Blood And Body Fluids: Despite the use of caution and personal protective equipment, unprotected exposure to a patient's blood or body fluids may occur. If an exposure occurs, personnel must report at once to OHS during normal business hours. If the exposure occurs after hours, the employee should report at once to the Emergency Department.

Stanford Hospital and Clinics Infection Control Manual Section 10.00

An "exposure" is defined as: Parenteral (e.g., needle stick or cut) exposure to any patient's blood or body fluids. Mucous membrane (e.g., splash to the eye or mouth) exposure to blood or other body fluids of any patients. A cutaneous exposure involving large amounts of blood or prolonged contact with blood, especially when the exposed skin is chapped, abraded or afflicted with dermatitis.

2. 3.

This post-exposure management includes confidential medical consultation, treatment, and counseling. The employee is offered the hepatitis B vaccine if nonimmune. The employee's and source patient's blood (if available) is tested for HBV, I ICV and HIV. Post-exposure prophylaxis is offered if indicated. All documents and records are confidential. The SHC Blood-bome Pathogen Exposure Control Plan contains detailed information and specific approaches developed to decrease the risk of occupational exposure to blood-borne pathogens. This document can be found in the SHC Safety Manual. Approved by: Infection Control Committee, 9/06 Quality Improvement and Patient Safety Committee, 10/06 Stanford Hospital and Clinics Medical Board, 11/06
Original Date: Reviewed Date: Revised Date: 7/91 8/93, 6/97, 1/98 9/06 7/27/ 1/01, 9/03, 2010 This document is intended for use by staff of Stanford Hospital and Clinics. No representations or warranties are made for outside use. Not for outside reproduction or publication without permission. Direct inquiries to: Infection Control and Epidemiology -- (650) 725-1106 Stanford Hospital and Clinics Stanford, CA 94305

D.

Precautions for Needles and Sharps

1. Use disposable needle electrodes and syringe tips whenever possible. Disposable items are used only once and then discarded in sharps container immediately after use Use only sterile needle electrodes for EMGs and Intra-operative Monitoring cases. All Intra-operative needle electrodes should be discarded in sharps container in the OR. Replace contaminated sharps containers when approximately' full. Wear gloves when inserting, removing or manipulating Needle electrodes or syringe tips Do not hold EMG needle electrode caps when recapping electrodes during patient procedures. Secure cap to the EMG instrument using Velcro strips. Place needle in cap when not in use: do not place on bed or dangle from amplifier box. Dispose of the entire needle-cap unit in sharps container.

2.

3. 4. 5.

E.

Surface Electrodes (EEG, NCS)

1.

2.

Use gloves for application, removal, and cleaning of electrodes. Cleaning and Disinfecting Surface Electrodes. Thoroughly clean electrodes with Exidine disinfecting solution and water after removal then dry with clean paper towel or cloth. Electrodes should then be placed in dry clean place (e.g. cabinet drawer) or hung, covered to prevent soiling.

F .

Reusable Intra-Operative Instruments

1. Sterilize all reusable Intra-operative instruments before use. These include BAER ear tubes, bipolar stimulator probes, NCV recording and stimulating electrodes, pedicle screw stimulating clips, and intracranial electrode cables. Use gloves to clean and prepare electrodes for processing. Wash the items with Exidine solution and water, then dry thoroughly. Process with STERRAD sterilization. Place item in sterilization pouch, drop in indicator strip, then seal pouch. Place first pouch inside second pouch, seal second pouch and apply piece of sterilization indicator tape to outside of pouch. Label outside of pouch with department name and identifying information.

2. 3.

G. H.

Electrolyte and Gels Personnel should use good judgment when using electrolyte past and gels directly from containers. Care should be taken not to contaminate containers with soiled hands, electrodes, or syringes. To avoid contamination a small amount of paste should be placed on a cloth, paper towel, and other small container or into a syringe. Dispose of the unused portions after completion of testing. Do not return unused portions back to the original containers.

I.

Creutzfeldt-Jakob Disease 1. Do not reprocess reusable needle or surface electrodes if CreutzfeldtJakob disease is suspected or diagnosed. Dispose of electrode and application items immediately after use in a contaminated sharps container or appropriate biohazard infectious waste bag.

2.

Use disposable surface electrodes for all suspected or diagnosed patients with Creutzfeldt-Jakob disease.

Stanford Hospital and Clinics

Infection Control Manual

Section 1.10

INFECTION CONTROL and PREVENTION PROGRAM I. PURPOSE

The Infection Control Program was developed to describe the comprehensive Stanford Hospital and Clinics (SHC) Program designed for the prevention and control of healthcareassociated infections (HAIs). The Infection Control Program is directed by the hospital epidemiologist (Infection Control Officer) and by the Infection Control Committee (ICC), and implemented by the Infection Control and Epidemiology Department (ICED). The Manager of the ICED has overall responsibility for assuring that SHC is in compliance with federal, state and county health agency regulations, recommendations, and SHC policies and procedures as they relate to the prevention of healthcare associated infections.

II.

POLICY
A. Infection Control and Prevention Program: 1 . Prevention and control of HAls are paramount responsibilities facing all healthcare facilities. SHC maintains an effective facility-wide program for the surveillance, prevention and control of infection. All patient care and patient support departments/services are included in the program. This Infection Control Program is guided by the ICC and implemented through the ICED. Since its inception in 1963 as the first U.S. hospital Infection Control Program, the SHC Infection Control Program has been at the forefront in defining the role of hospital infection control programs. The current Infection Control Program encompasses surveillance, education and consultation activities. The Manager and staff of the ICED are responsible for surveillance, education and consultation activities as they relate to the identification and prevention of healthcare associated infections. 3. The goal of the SHC Infection Control Program is to reduce the risk of acquisition and transmission of HAIs. SHC achieves this goal by: a. Incorporating the Infection Control Program as a major component of the safety and performance improvement programs. b. Performing an ongoing assessment to identify risks for the acquisition and transmission of infectious agents. c. Using an epidemiologic approach that consists of surveillance, data collection and trend identification. d. Effectively implementing infection prevention and control processes. e. Educating and collaborating with hospital-wide leaders to effectively encourage participation in the design and implementation of the Infection Control Program. f. Integrating its efforts with healthcare and community leaders to the extent practicable, recognizing that infection prevention and control is a community-wide effort.

Stanford Hospital and Clinics Infection Control Manual

Section 1.10

g .

By remaining a viable community resource, SHC has plans in place for responding to infections that could potentially overwhelm its resources.

4.

The following components comprise the Infection Control Program at SHC: a. The hospital epidemiologist (Infection Control Officer) or designee has the authority to take steps to prevent or control the acquisition and transmission of infectious agents. b . All applicable organizational components and functions are integrated into the Infection Control Program c. Systems are in place to communicate with licensed independent practitioners, staff, students/trainees, volunteers and as appropriate, visitors, patients and families about infection prevention and control issues, including their responsibilities in preventing the spread of infection within the hospital. d. The hospital has systems for reporting infection surveillance, prevention and control information to the following: 1) The appropriate staff within the hospital. 2) Federal, state and local public health authorities in accordance with law and regulations. 3) Accrediting bodies. 4) The referring or receiving organization when a patient was transferred or referred, and the presence of an HAI was not known at the time of transfer or referral. e. Systems for the investigation of outbreaks of infectious diseases are in place. f Applicable policies and procedures are in place throughout the hospital. g. The hospital has a written infection control plan that includes the following: 1) A description of prioritized risks. 2) A statement of the goals of the Infection Control Program. 3) A description of the hospital's strategies to minimize, reduce or eliminate the prioritized risks. 4) A description of how the strategies are evaluated. h. The hospital identifies risks for the transmission and acquisition of infectious agents throughout the hospital based on the following factors: 1) The geographic location and community environment of the hospital, program/services provided and the characteristics of the population served. 2) The results of the analysis of the hospital's infection prevention and control data. 3) The care, treatment and services provided. i . The risks analysis is formally reviewed at least annually and whenever significant changes occur in any of the above factors.
-2-

Stanford Hospital and Clinics

Infection Control Manual

Section 1.10

j.

k.

1 .

Surveillance activities, including data collection and analysis are used to identify infection prevention and control risks pertaining to the following: 1) Patients. 2) Licensed independent practitioners, staff, volunteers and students/trainees. 3) Visitors and families, as warranted. Priorities are established and goals related to preventing the acquisition and transmission of potentially infectious agents are developed based on the risks identified. Goals include, but are not limited to the following: I) Limiting unprotected exposure to pathogens throughout the hospital. 2) Enhancing hand hygiene. 3) Minimizing the risk of transmitting infections associated with the use of procedures, medical equipment and medical devices. Interventions are designed to incorporate relevant guidelines for infection prevention and control activities. Interventions are implemented which include the following: 1 ) A hospital-wide hand hygiene program that complies with current Centers for Disease Control and Prevention (CDC) hand hygiene guidelines (National Patient Safety Goal 7, requirement 7.a). 2 ) Methods to reduce the risks associated with procedures, medical equipment and medical devices, including the following: a) Appropriate storage, cleaning, disinfection, sterilization and/or disposal of supplies and equipment. b) Reuse of equipment designated by the manufacturer as disposable in a manner that is consistent with regulatory and professional standards. c) The appropriate use of personal protective equipment. 3) Implementation of applicable precautions, as appropriate, is based on the following: a) The pot ent ial for tr an s mi ssion . b) T h e me c h a n i s m o f t r a n s mi ssio n . c) The care, treatment and service setting. d) The emergence and reemergence of pathogens in the community that could affect the hospital. 4) Screening for exposure and/or immunity to infectious diseases that licensed independent practitioners, staff, student/trainees and volunteers may come in contact with in their work is available as warranted. 5) Referral for assessment, potential testing, immunization and/or prophylaxis/treatment, and counseling as appropriate

Stanford Hospital and Clinics Infection Control Manual Section 1.10

6)

of licensed independent practitioners, staff, students/trainees and volunteers who are identified as potentially having an infectious disease or risk of infectious disease(s) that may put the population they serve at risk. Referral for assessment, potential testing, immunization and/or prophylaxis/treatment, and counseling as appropriate of patients, students/trainees and volunteers who have been exposed to infectious disease(s) at the hospital and licensed independent practitioners or staff who are occupationally exposed.

m.

n.

Reduction of risks associated with animals brought into the hospital. Immunization against influenza is offered to staff and licensed independent practitioners. 1) The Influenza Vaccination Program is established annually. 2) Access to influenza vaccination is provided onsite. 3) Staff and licensed independent practitioners are educated about: a) Influenza vaccination. b) Non-vaccine control measures (such as the use of appropriate precautions). c) The diagnosis, transmission and potential impact of influenza. 4) Vaccination rates and reasons for non-participation in the hospital's immunization program are evaluated annually. 5) Enhancements are implemented to increase participation in the Program. The hospital formally evaluates and revises the goals and program (or portions of the program) at least annually and whenever risks significantly change. 1) The evaluation addresses changes in the scope of the Infection Control Program (for example, resulting from the introduction of new services or new sites of care). 2) The evaluation addresses changes in the results of the Infection Control Program risk analysis. 3) The evaluation addresses emerging and reemerging problems in the healthcare community that potentially affect the hospital (for example, highly infectious agents). 4) The evaluation addresses the assessment of the success or failure of interventions for preventing and controlling infection. 5) The evaluation addresses responses to concerns raised by leadership and others within the hospital. 6) The evaluation addresses the evolution of relevant infection prevention and control guidelines that are based on evidence or, in the absences of evidence, expert consensus.

7)

Stanford Hospital and Clinics Infection Control Manual

Section 1.10

o.

P .

q .

r .

s.

. t

The hospital plans its response to an influx or risk of an influx of infectious patients. I) The hospital has a plan for managing an ongoing influx of potentially infectious patients over an extended period. The hospital does the following: a) Determines how to keep abreast of current information about the emergence of epidemics or new infections which may result in the hospital activating its response. h) Determines how to disseminate critical information to staff and other key practitioners. c) Identifies resources in the community (through local, state and/or federal public health systems) for obtaining additional information. Hospital leadership has assigned responsibility for oversight and coordination of the development, testing and implementation of evidence-based practices to prevent healthcare-associated infections due to multiple drug-resistant organisms to the SHC ICED. Hospital leadership has assigned responsibility for oversight and coordination of the development, testing and implementation of best practices or evidence-based guidelines to prevent central lineassociated bloodstream infections to the SHC ICED. Hospital leadership has assigned responsibility for oversight and coordination of the development, testing and implementation of best practices for preventing surgical site infections to the Department of Surgery, in consultation with the SHC ICED. SHC has assigned responsibility for managing Infection Control Program activities to the Manager of the ICED and three Infection Control Nurses whose number, competency and skill mix are determined by the goals and objectives of the Infection Control Program activities. I ) Qualifications of the individual(s) responsible for managing the Infection Control Program are determined by the risks entailed in the care, treatment and services provided to the SHC patient population and the complexity of the activities that are carried out. 2) These individuals coordinate all infection prevention and control activities within the hospital and clinics. 3) These individuals facilitate ongoing monitoring of the effectiveness of prevention and/or control activities and intervention. Hospital leaders, with licensed independent practitioners, medical staff, and other direct and indirect patient care staff including, when applicable, Administration, Building Maintenance/Engineering, Food Services, Housekeeping, Clinical Microbiology Laboratory, Pharmacy and Sterilization Services, collaborate on an ongoing basis

Stanford Hospital and Clinics Infection Control Manual

Section 1.10

u.

with the qualified individual(s) managing the Infection Control Program. These representatives participate in the following: 1) Development of strategies for each component's/function's role in the Infection Control Program. 2) Assessment of the adequacy of the human, information, physical and financial resources allocated to support infection prevention and control activities. 3) Assessment of the overall failure or success of key processes for preventing and controlling infection. 4) The review and revisions of the Infection Control Program as warranted improving outcomes. The effectiveness of the hospital's infection prevention and control activities is reviewed on an ongoing basis, and findings are reported to the integrated patient safety program at least annually. 1) Adequate systems to access information are provided to support infection prevention and control activities. 2) Adequate laboratory support is provided to support infection prevention and control activities. 3) Adequate equipment and supplies are provided to support infection prevention and control activities.

B.

Structure of the Program: 1. Surveillance: Focused surveillance, including the identification and tracking of nosocomial infections and problems, and the monitoring for necessary corrective actions, is done by the ICED staff to determine the types and frequency of surveillance of targeted nosocomial infections, and to identify procedures and practices associated with high risk for acquiring infections. 2. Sentinel Events: a. All patients included in the focused surveillance program are followed for patient outcome 30 days post healthcare-acquired infection. If the outcome is unanticipated death or major permanent loss of function associated with a healthcare-acquired infection, the case is forwarded to the Quality Improvement and Patient Safety Department (QIPSD). Those cases identified by QIPSD screening as requiring ICED review are included. b. In cases identified as a sentinel event, the QIPSD initiates a root cause investigation, and includes a member of the ICED on the team. Education: An education program is in place to ensure implementation of infection control measures and to provide feedback to healthcare workers about nosocomial infections. Infection control is a multi-disciplinary

Stanford Hospital and Clinics Infection Control Manual

Section 1.10

responsibility; thus the educational programs include classes for medical, nursing and paramedical personnel, as well as patient instruction. 4. Consultation: Consultation services regarding the principles and techniques pertinent to infection control are available to all departments. Preventive as well as problem-solving techniques are devised using the expertise of hospital departments and ICED staff. 5. Policy and Procedure Activities: a. The ICED assists and supports SHC patient care units and departments with design and implementation of appropriate unit/department-specific infection control policies. b. This process incorporate guidelines/regulations/standards of associated agencies and organizations (e.g., Centers for Disease Control and Prevention, Association for Professionals in Infection Control and Epidemiology, State of California Department of Health Services, Joint Commission on Accreditation of Healthcare Organizations) and of SHC into department-specific infection control policies and procedures. Responsibility: a. All department managers and their staff are responsible for knowing and implementing the hospital and departmental policies and procedures designed to facilitate the Infection Control Program. It is only through knowledge and the cooperative effort of each member of the staff that nosocomial infections can be prevented. Any questions or concerns about nosocomial infection control and prevention should be directed to the Manager and staff of the ICED. b. The Infection Control Program shall set forth written policies and procedures for infection surveillance, prevention and control for all patient care departments and services. The Infection Control Program includes policies and procedures which address the following: 1) The required methods for handling all blood and body fluids to reduce risk of transmission of potentially infectious microorganisms from patient to patient and between patient and healthcare worker. Such methods shall include, as appropriate, hand washing, use of gloves, use of other barriers, handling of needles/sharps and disposal of materials soiled with or containing blood and/or body fluids; 2) The required practices to reduce risk of transmission of airborne infectious etiologic agents, including the assignment of rooms and/or roommates; The required indications for specific precautions to prevent transmission of infection, including the requirement that

6 .

3)

Stanford Hospital and Clinics Infection Control Manual

Section 1.10

4)

adequate infection control devices and supplies be available in patient care areas and filled waste containers be disposed of in a timely manner in accordance with the Hospital/Clinic's hazardous materials and waste program, The required provisions for the education of personnel, the program shall provide for the training/education of each new employee as to the infection control policies and procedures of the Hospital/Clinics, require that training materials be kept current to conform with new information pertaining to prevention and control of infectious diseases, and require that personnel be provided with revised training materials. Documentation of training is maintained by the managers of each department; The required plan for surveillance, prevention and control of nosocomial infections and procedures for investigation and management of outbreaks.

5)

C.

Infection Control Committee: Responsibilities: The ICC, which meets at least four times a year and more frequently as necessary, oversees, in conjunction with the ICED, the program for surveillance, prevention and control of infection for SHC' departments/services, medical and nursing staffs, and administration. The scope of this commitment includes care of patients, personnel health, and the environment. The ICC and the ICED oversee the SHC Infection Control Program as follows: a. Evaluate and approve the type and scope of surveillance activities, based on trend analysis of surveillance, effectiveness of prevention and control measures and procedures instituted; Approve actions to prevent or control infection, based on evaluation of trends and analysis of nosocomial infections and of the infection potential among patients and hospital personnel; Review nosocomial infections where there is potential for prevention or intervention to reduce the risk of figure occurrence. Special focus is given to infections due to unusual pathogens and clusters; Review and approve, as least every three years, all policies and procedures related to the infection surveillance, prevention, and control program. Oversee infection surveillance, prevention, and control activities in all departments/services; Assist Occupational Health Services (OHS) in formulating and evaluating policies and procedures regarding exposures and communicable diseases among employees; Review and evaluate plans for renovation of existing facilities and plans for construction of new facilities to incorporate sound infection control principles into the design and to promote implementation of
-8-

b.

c.

d.

e.

f.

Stanford llospital and Clinics Infection Control Manual

Section 1.10

aspergillosis prevention policies and monitoring compliance systems in all phases of construction/renovation plans.
2

Membership: a. Committee membership is interdisciplinary and includes representatives from Administration, Medical Staff, Patient Care Services, Clinical Microbiology Laboratory, OHS and the ICED. Representatives from other departments/services serve on the ICC on an ad hoc basis. b. Representation from Housekeeping, Materials Management, Laundry, Nutrition and Food Service, Pharmacy and Operating Room Services may be included on the Committee, as needed, to provide information or expertise to the Committee. c. Members of the ICC are responsible for: 1) Bringing clinical, administrative or epidemiological expertise to the Committee; 2) Participating in data evaluation; and 3) Reviewing and approving infection control policies and procedures. Authority: a. The Medical Director (Infection Control Officer) of the SHC Infection Control Program or a designated representative has authority to institute any surveillance, prevention, and control measures or studies when there is reason to believe that any patient or personnel may be in danger. This includes excluding when necessary, an employee or staff member from patient contact. This statement of authority is reviewed and approved every three years by the Medical Board of SHC. b. The Medical Director (Infection Control Officer) of the SHC Infection Control Program or a designated representative shall: 1) Serve as Director of the Infection Control Program. 2) Serve as Chairperson of the ICC. 3) Have the authority to establish policy, surveys, or regulations in the face of real or potential threats to the health and safety of patients and personnel. When such action is warranted, appropriate staff are promptly notified. 4) Request individual compliance with existing infection control policies, criteria, or regulations. 5) Have access to all relevant patient records, and when it deems advisable, shall consult with the patient's physician or designated individual. 6) Submit an annual report to the Quality Improvement and Patient Safety Committee and the Medical Board concerning current activities of the ICED and ICC.

3 .

tanford Hospital and Clinics

Infection Control Manual Section I.10

7)

As the designated representative of the Hospital, cooperates with local, state, and national health agencies in the study and control of infection.

4 .

Committee Minutes: a. Conclusions, recommendations, and actions are documented in the minutes of the Committee meetings. b. The minutes are forwarded to members of the ICC, the Quality Improvement and Patient Safety Committee and the Medical Board. c. The responsibility for taking action on the recommendations documented in the minutes is assigned and defined in writing. d. Reviews and approvals are documented in the minutes of the Committee meetings.

References: Joint Commission, Accreditation Program: Hospital Chapter National Patient Safety Goals 2009.
Appendices:

Appendix A: Sentinel Event Monitoring Process for Unanticipated Death Approved by: Infection Control Committee, 1/09 Quality Improvement and Patient Safety Committee, Stanford Hospital and Clinics Medical Executive Committee, Stanford Hospital and Clinics Board Credentials, Policies and Procedures Committee,
Original Date:

9/87 Reviewed Date: 2/94,1/01 Revised Date:3/91, 2/96, 1/98, 9/03, 12/05, 11/06, 1/09, 7/27/2010

Review and coordinate

QIPSD

' -

Sentinel Event Monitoring Process for Unanticipated Death Associated with a Healthcare-Acquired Infection

Infection Control Department Monitoring

(

C
___ ]

QIPSD Monitoring

Conduct focused surveillance 30 days after infection notedreview for patient outcome

- Selected Infection - Post-op Sepsis - Death and Low Mortality DRGs

Case reviewed by QIPSD

Na further followup - No L necessary

continue to monitor

Yes

Yes

Identify if outcome is associated with healthcare-acquired infections

Infection Control notified to conduct/review case

No further follow-up necessary

No

HContinue monitor

to

Yes

Yes

Notify Risk Management Root

Notify Risk Management

Cause

Analysis (RCA) Case reviewed at Care Review Committee Reported to QIPSC

-10 - 12

Stanford Hospital and Clinics Infection Control Manual

Section 1.30

INFECTION CONTROL RESPONSIBILITIES FOR DEPARTMENT MANAGERS I . PURPOSE Stanford Hospital and Clinics (SHC), through the Infection Control and Epidemiology Department (ICED) maintains an effective hospital-wide program for the surveillance, prevention, and control of infection. All patient care and patient support departments/ services are included in the program. Department managers are responsible for ensuring a safe environment for patients, personnel and visitors. Employees, housestaff, students and volunteers are responsible for complying with Infection Control Manual (ICM) policies and procedures in the performance of their duties. An essential part of this program incorporates patient infection prevention and control measures, as well as systems of barrier precautions to be used by ALL personnel for contact with blood, body fluids, and non-intact skin of ALL patients, regardless of the patient's diagnosis. In the implementation of this approach, personnel must assess the anticipated exposure to blood, body fluids and non-intact skin of any patient. IL POLICY A. Each manager or designee of a patient care unit, hospital department or clinic reviews the employee's requirements (refer to policy 1.40 in the /CM) and instructs each employee in the employee's role in the prevention of infection and the scope of their responsibilities in preventing infection. Each manager of a patient unit, hospital department or clinic incorporates infection prevention and control practices into departmental policies and procedures in order to reduce the risk of healthcare-associated infections. Each manager or designee of a patient care unit, hospital department or clinic assures that hand hygiene is performed upon entry into a patient or clinic room, upon ext from a patient or clinic room, and after removal of gloves. All staff must complete and sign the Hand Hygiene Pledge on hire. Educational programs reviewing principles of infection control are given to current and newly hired employees. Documentation of training is maintained via Healthstream. ICED staff are available to present programs and consult with managers regarding infection control topics not included in Healthstream. Each manager or designee of a patient care unit, hospital department or clinic supervises employees in infection control and prevention practices, evaluates the need for further training and provides training as needed in consultation with the ICED. Compliance with hand hygiene and Isolation Precautions are incorporated into the individual's annual employee performance appraisal.

B.

C.

D.

E.

Approved by: Infection Control Committee, 5/08 Quality Improvement and Patient Safety Committee, 7/08 Stanford Hospital and Clinics Medical Executive Committee, 8/08
Original Date: 7/91 Reviewed Date: 8/93, 1/98 Revised Date:6/97, 1/01, 5/03, 10/05, 5/08, 7/27/2010

Stanford Hospital and Clinics Infection Control Manual

Section 1.40

INFECTION CONTROL RESPONSIBILITIES FOR EMPLOYEES, HOUSESTAFF, STUDENTS AND VOLUNTEERS

1 .

PURPOSE
Stanford Hospital and Clinics (SHC), through the Infection Control and Epidemiology Department (ICED) maintains an effective hospital-wide program for the surveillance, prevention, and control of infection. All patient care and patient support departments/ services are included in the program. Department Managers are responsible for ensuring a safe environment for patients, personnel and visitors. Employees, housestaff, students and volunteers are responsible for complying with Infection Control Manual policies and procedures in the performance of their duties. An essential part of this program incorporates patient infection prevention and control measures, as well as systems of barrier precautions to be used by ALL personnel for contact with blood, moist body substances, and non-intact skin of ALL patients, regardless of the patient's diagnosis. In the implementation of this approach, personnel must assess the anticipated exposure to blood, body substances and non-intact skin of any patient.

II. IMPLEMENTATION
A. Responsibilities 1. All employees, housestaff, students and volunteers (referred to as personnel) must comply with infection control policies and procedures to minimize the risk of transmission of nosocomial (hospital-associated) infections to patients and personnel. Perform hand hygiene before and after contact with each patient contact, before performing each invasive procedure, before contact with food, after contact with patient's body fluids, after removing gloves, after using rest rooms, and before and after contact with eyes, nose or mouth. Consume food or liquid in designated locations away from patient care areas, charting areas, or specimen holding areas to prevent the risk of acquiring gastrointestinal infection caused by microorganisms which may be present in the patient environment. Cover non-intact skin with band-aids or other impermeable covering. Wear gloves for contact or anticipated contact with any patient's body fluids, mucous membranes or non-intact skin, and for handling items moist with body fluids. Remove the gloves and perform hand hygiene immediately upon completion of each individual procedure requiring gloves. A new pair of gloves must be used for each task on the same patient. Wear a mask and protective eye-wear when splatter or aerosolization of blood or body fluids is anticipated. Wear a gown when there is close contact with a patient's non-intact skin and when it is likely that your clothing is soiled with a patient's body fluids. Do not report to work until symptoms are no longer present if you have draining skin lesions, rash, flu-like symptoms (e.g., sore throat with fever, arthralgia) or an acute diarrheal illness. -1-

2.

3.

4. 5.

6. 7. 8.

Stanford Flospital and Clinics Infection Control Manual

Section 1.40

9 .

10.

11. 12.

13.

14.

5 .

16.

17.

Use single dose medication vials or single use pre-filled syringes to flush IV lines/saline locks to prevent transmission of microorganisms during re-entry into multi-dose vials. Access multiple dose medication vials using sterile technique. Do not take multi-dose vial into patient room or exam room. Discard vials if contamination has occurred during use of vial(s), if contents appear cloudy or vial is cracked and when manufacturers' expiration date on the label has passed. When accessing insulin, use aseptic technique and keep vial refrigerated at the medicine station. Sterile items processed at SHC do not have an expiration date. Sterile items must be inspected by the user before the package is opened. If the package is torn, wet, has a broken seal or is otherwise damaged, it is not to be used. If contaminated item is disposable, it must be removed from use and returned to Materials Management. If contaminated item is reusable, return item to Supply Processing for inspection and reprocessing. Commercially sterilized packages and crash cart modules that contain materials that become outdated (e.g., medication, batteries) are dated with an expiration date. Store refrigerated medications, food products and patient specimens in separate refrigerators. Use safety syringes, needles and other sharps to prevent bloodbome pathogen exposure. (Refer to Safety Sharp Devise Use policy in the Health and Safety Manual.) Dispose of attached needle and syringe in puncture-resistant containers. When the container is three-fourths full, the container should be sealed and replaced with a new one, to prevent injury from needles protruding from a "too-full" container opening. Handle all patient specimens as if they contain biohazardous material, including wearing gloves and placing specimens in impermeable plastic bags immediately after obtaining specimen. Handle all soiled linen in the same careful manner, including wearing gloves when linen is contaminated with body fluids and placing soiled linen in moisture proof plastic bags. a. Handle all soiled linen in a manner that prevents skin and mucous membrane exposures and contamination of clothing, and avoids transfer of microorganisms to other patients and environmental surfaces. b. Wear gloves when linen is contaminated with body fluids. c. Place soiled linen in a regular linen hamper. Do NOT put soiled linen in red infectious waste bags. d. Soiled linens from isolation rooms are placed in regular soiled linen bags. Use disposable electronic thermometer covers for taking temperatures for each patient. Clean electronic thermometer base daily with a hospitalapproved disinfectant wipe. Use disposable equipment for one patient only (and for one time only, if so stated by the manufacturer), and then discard in the appropriate receptacle.

Stanford Hospital and Clinics Infection Control Manual

Section 1.40

13.

19.

20.

21. 22. 23.

24.

Place contaminated reusable patient care instruments or equipment in designated containers. Send to Sterile Reprocessing for decontamination and reprocessing by trained personnel. Assure that the disposable resuscitation bags with disposable mouth pieces for use during emergency mouth-to-mouth resuscitation are readily available in each patient care area. Personnel are advised to use disposable mouth pieces during resuscitation efforts. Dispose of patient care equipment that contains liquid blood (e.g., pleurovacs, blood administration bags, tubing containing liquid blood) in waste container labeled "Biohazardous Waste". Instruct patients on infection control concepts, such as the proper use of tissues and appropriate hand hygiene technique, when indicated. Place patients who soil their environment with moist body substances in private rooms. Review policy 5.10 of the Infection Control Manual for instruction on management of patients with specific diseases requiring precautions or isolation. Contact the ICED (extension 5-1106 or pager 16167) when a patient is on Respiratory or Contact Precautions.

B .

Employee, Housestaff, Student and Volunteer Immunity and Immunizations

I.

2.

3.

Personnel must be vaccinated against or immune to measles and rubella. Personnel should contact Occupational Health Services (OHS) to determine their immunity to chicken pox. Personnel who are not immune to chicken pox and have household exposure to a person with the infection must contact OHS immediately after such infection is diagnosed in a household member. Immunizations to measles, rubella and chicken pox are provided free of charge through OHS. Personnel who have a household exposure to a communicable disease (e.g. mumps, meningococcal meningitis, tuberculosis, SARS) must contact OHS immediately after such infection is diagnosed in a household member. Personnel who have contact with blood and body fluids should be immunized against hepatitis B virus infection if not already immune, or sign a Vaccination Declination Statement. Personnel may obtain this immunization from OHS.

C.

Post-Exposure Follow-Up For Employees Exposed To Blood And Body Fluids (see Blood-bome Pathogen Exposure Control Plan in the Health and Safety Manual) 1. Despite the use of caution and personal protective equipment, unprotected exposure to a patient's blood or body fluids may occur. If an exposure occurs, personnel must report at once to OHS during normal business hours. If the exposure occurs after hours, the employee should report at once to the Emergency Department. An "exposure" is defined as: a. Parenteral (e.g., needle stick, cut) exposure to any patient's blood or body fluids.
-3

2.

Stanford Hospital and Clinics Infection Control Manual

Section 1.40

3.

4.

Mucous membrane (e.g., splash to the eye or mouth) exposure to blood or other body fluids of any patients. c. A cutaneous exposure involving large amounts of blood or prolonged contact with blood, especially when the exposed skin is chapped, abraded or afflicted with dermatitis. This post-exposure management includes confidential medical consultation, treatment and counseling. The employee is offered the hepatitis B vaccine if non-immune. The employee's and source patient's blood (if available) are tested for HBV, FICV and HIV. Post-exposure prophylaxis is offered if indicated. All documents and records are confidential. The SIIC Blood-bome Pathogen Exposure Control Plan contains detailed information and specific approaches developed to decrease the risk of occupational exposure to blood-bome pathogens. This document can be found in the RIC Health and Safety Manual.

b.

Approved by: Infection Control Committee, 11/07 Quality Improvement and Patient Safety Committee, 1/08 Stanford Hospital and Clinics Medical Board, 2/08
Original Date: 7/91 Reviewed Date: 8/93, 1/98 Revised Date: 6/97, 1/01, 9/03, 10/05, 9/06, 10/07 This document is intended for use by staff of Stanford Hospital and Clinics. No representations or warranties are made for outside use. Not for outside reproduction or publication without permission. Direct inquiries to: Infection Control and Epidemiology -- (650) 725-1106 Stanford Hospital and Clinics Stanford, CA 94305

TECHNOLOGIST

DATE

NEURODIAGNOSTIC LABS STANFORD HOSPITAL AND CLINICS END TECHNOLOGIST COMPETENCY CHECKLIST The Electroneurodiagnostic Technologists are evaluated for competency in performing Electroencephalograms in the areas of basic knowledge, technical and clinical performance and quality of patient care. The competency measurement process is a dynamic one involving observation of technologists performance on a daily basis. In addition the yearly performance appraisal of technologists is built around the competency criteria. QUALITY OF PATIENT CARE COMPETENCIES: Verifies identity of patient Explains all tests procedures including activations Explains electrode application Interacts with patient on an appropriate level for age and mental capacity. Attends to patient needs appropriately Removes electrode paste/glue from the patient's scalp and hair. Is able to achieve patient relaxation and cooperation through personal communication

Treats patient with respect throughout the procedure Guards patient confidentiality Follows lab and hospital precautions for infection prevention Exhibits proper actions to insure patient safety with a clinical seizure

BASIC EEG COMPETENCIES: Gathers pertinent patient history Notes patient's mental, behavioral, and consciousness states Measures and marks head accurately and proficiently using the 10/20 International Electrode Placement System Adjusts electrode placement for anatomical defects or anomalies Preps patient's scalp prior to electrode application A pplies electrodes accurately and proficiently using paste or collodian Obtains electrode impedances that are below 5k ohms and balanced. Is able to calibrate system amplifiers Checks system setting including filters, sensitivity, time base

Performs at least 20 minutes of technically acceptable recording

END TECHNOLOGIST COMPETENCY CHECKLIST

Includes eye opening and closing in recording Notes on recording patient movements and behaviors Is able to distinguish artifactual waveforms from real EEG data Corrects artifactual electrodes promptly Assess patient level of consciousness Has patient perform 3 minutes of hyperventilation or determines if hyperventilation is contraindicated Performs photic stimulation at frequencies appropriate for history and reactivity. Selects appropriate setting changes to allow best interpretation of data and enhancement of any recognized abnormalities Describes in detail any clinically significant behavior during EEG Is able to troubleshoot for causes of electrical interference. Fills out tech sheet with pertinent information Enters patient information into EEG log Is able to transfer digital EEG data over network to physician reading station Prepares billing sheet with appropriate information

CLINICAL EEG COMPETENCIES: Can recognize normal awake and sleep patterns for each age range. Can recognize abnormal awake and sleep patterns for each age range Understands functional neuroanatomy and neurophysiology Understands International Classification of Seizures Understands seizure manifestations and EEG waveform correlates Can recognize clinical seizure patterns Knows effects of medications on EEG background and waveforms Understands medical terminology and accepted abbreviations as they apply to EEG Understands signs, symptoms and EEG correlates for adult neurological disorders Understands signs, symptoms and EEG correlates for pediatric neurological disorders Can recognize EEG patterns for levels of consciousness

TECHNICAL EEG COMPETENCIES: Understands and follows technical criteria for recording adult EEGs understands and fodows technical criteria for recording pediatric EEGs Understands and follows technical criteria for recording neonatal EEGs Understands and follows technical criteria for recording electrocerebral silence EEG ( ECS) Understands and follows technical criteria for recording EEG in the ICU. Understands how differential amplifiers work

END TECHNOLOGIST COMPETENCY CHECKLIST Understands the principles of EEG polarity Is able to measure the voltage and duration of a waveform Understands analog to digital conversion Knows how filter, sensitivity, and paper speed setting affect waveforms Understands the difference and usage of referential and bipolar montages Understands the affect of a notch filter (60Hz filter) on waveforms Knows how waveforms are affected by different electrode types and electrode compositions Knows how to use voltmeter to test for electrode integrity Is able to utilize technical techniques to bring out or enhance EEG abnormalities Recognizes the need to apply additional electrodes to localize abnormal activity Recognizes the need to apply physiological monitoring electrodes to aid in interpretation

END TECHNOLOGIST COMPETENCY CHECKLIST EPILEPSY MONITORING The following are additional competencies that should be exhibited by technologists working in the epilepsy monitoring unit. These technologists must meet all of the competencies outlined above for the general END Technologist.

PATIENT SETUP:
Understands electrode color coding Correctly labels and double-checks ribbon cables for Phase II patients Is able to setup supplies and assist nurses with sterile dressing changes Is able to assess implanted electrode site for abnormal discharge and irritation Properly labels any additional electrodes or monitors that are used Is proficient at head wrapping techniques Is able to assist physician in insertion of sphenoidal electrodes Properly selects inputs in amplifiers Properly labels amplifiers Understands how to jumper Preamplifiers together when more than one is used. Correctly sets up encoder or digiplex Thoroughly explains the video EEG procedure to patient Instructs patient and/or family member on use of the event bulb Instructs patient and/or family member on use of the dayroom Instructs patient and/or family member on safety issues, especially Phase 2 patients

RECORDING SYSTEM SETUP:

Can start video EEG recording Can start video EEG recording Can setup Phase II protocol and montages Can manipulate the camera controls to obtain best video picture of patient. Can start recording on Seizure Detection computer Understands parameter changes and their affect on seizure detection storage. Can setup recording systems for sequenced recordings (16 hr) Can create new montages for recording and seizure detection systems. Labels storage media appropriately Sets up log sheet on new patients

DATA PLAYBACK AND REVIEW: Is able to scan through recorded material to find significant events Can identify spikes and seizure activity in the EEG Can identify clinical seizure activity in patients Knows how to playback recorded data on seizure detection computers Knows how to transfer data from seizure detection computers to the local area network Is able to use the equipment to produce printouts EDITING AND ARCHIVING OF DATA:

Is able to edit significant data from recorded media to the network and archived material Is able to edit significant data to save from raw seizure detected data Archives hardcopy printouts, labeling boxes appropriately

STANFORD HOSPITAL AND CLINICS AGE SPECIFIC COMPETENCY ASSESSMENT: NEURODIAGNOSTIC LAB
Name: Position: Date: Evaluator:

brain.

Job Summary: Performs EEGs, Ambulatory EEGs, and Long Term Monitoring for Epilepsy to evaluate the electrical activity of the

Age Range of Patients to Whom Service is Provided: Neonate to Geriatric

DEMONSTRATES SKILLS NEEDED FOR AGE SPECIFIC CARE NEONATE/INFANT(Newborn to 1 Year) Demonstrates ability to record appropriate EEG recording on neonate utilizing: - modified head electrode placement - physiological monitors (EOG,EMG,RESP) - modified instrument settings Demonstrate knowledge of normal EEG activity in neonates, including sleep cycles. Able to recognize abnormal EEG activity in neonates including neonatal seizure activity. Demonstrate knowledge of maturation of normal EEG activity from neonate age to 1 year of age Maintains safe environment for infant: maintain warmth, crib rails in "up" position and locked, infant not left unattended at any time. Demonstrate safe handling of infant during lift, carry, and transport. Demonstrate ability to perform EEG on infant in isolette, warming bed; skills to troubleshoot "noise" problem in ICU environment Explains EEG procedure to parents and involves them in the recording. Uses distraction methods to calm infant including providing stimulating objects.

MET

FF

N/A

COMMENTS

Approaches and provides care in calm, tender, soothing manner.

DEMONSTRATES SKILLS NEEDED FOR AGE SPECIFIC CARE PEDIATRICS: 1 TO 3 YEARS

MET

NOT MET

N/A

COMMENTS

Demonstrates ability to record appropriate EEG recording on infant utilizing: - standard head electrode placement - appropriate instrument settings Demonstrate knowledge of normal and abnormal EEG activity in infants, including seizure activity. Demonstrate knowledge of maturation of normal EEG activity from age 1 to 3 years. Maintains safe environment for infant: crib or bed rails in "up" position and locked, infant not left unattended at any time. Demonstrate safe handling of infant during lift, carry, and transport. Allows child to become accustomed to environment; approaches child in calm manner Uses praise as a reward for positive attitude and behavior; uses touch as a form of comfort, as appropriate to child's needs and reactions Explains EEG procedure to parents and involves them in the recording; keeps parents within patient's view during the procedure.
PEDIATRICS: 3 TO 11 YEARS

Demonstrates ability to record appropriate EEG recording on child utilizing: - standard head electrode placement - appropriate instrument settings Demonstrate knowledge of normal and abnormal EEG activity in this age group, including seizure activity. Explain procedure in age appropriate language to child's level of understanding; use demonstration methods to explain procedure

DEMONSTRATES SKILLS NEEDED FOR AGE SPECIFIC CARE

MET

NOT MET

N/A

COMMENTS

Demonstrate sensitivity to child's fears and apprehensions; involve child in procedure. Uses praise as a reward for positive attitude and behavior; uses touch as a form of comfort, as appropriate to child's needs and reactions. Explains EEG procedure to parents and involves them in the recording if necessary; keeps parents within patient's view during the procedure. Maintains safe environment for child: bed rails in "up" position and locked position
ADOLESCENTS: 12 TO 19 YEARS Demonstrates ability to record appropriate EEG recording on adolescent age group utilizing: - standard head electrode placement - appropriate instrument settings - appropriate activation procedures Demonstrate knowledge of normal and abnormal EEG activity in this age group, including seizure activity.

Explain procedures to patient before they are performed using logical sequence of steps; explain in language patient can understand Involve patient in care and procedure. Allows time for and encourages questions; encourage verbalization of fears; allows patient to have choices and control over situation as appropriate to the recording. Keep parents informed as needed. Maintains privacy during the procedure Maintains safe environment for patient: bed rails in "up" position and locked position

DEMONSTRATES SKILLS NEEDED FOR AGE SPECIFIC CARE

MET

NOT MET

N/A

COMMENTS

ADULT: 19 TO 65 YEARS Demonstrates ability to record appropriate EEG recording on adult age group utilizing: - standard head electrode placement - appropriate instrument settings - appropriate activation procedures if no contraindications Demonstrate knowledge of normal and abnormal EEG activity in this age group, including seizure activity. Maintain safe environment for patient related to equipment, bed rails, mental status. Explains procedure and rational for testing to patient and/or family prior to recording at a level of understanding appropriate to their comprehension level. Involves patient in care and procedure if appropriate; involves patient in decision-making as appropriate to conditions and situation. Encourages verbalization of fears and anxiety; encourages questions. GERIATRIC: 65 + Demonstrates ability to record appropriate EEG recording on geriatric age group utilizing: - standard head electrode placement - appropriate instrument settings - appropriate activation procedures if no contraindications Demonstrate knowledge of normal and abnormal EEG activity in this age group, including seizure activity. Maintain safe environment related to equipment, bed rails, fall precautions, mobility needs and mental status; institutes appropriate preventative measures. Explains procedure and rational for testing to patient and/or family prior to recording at a level of understanding appropriate to their comprehension level. Involves patient in care and procedure if appropriate; involves patient in decision-making as appropriate to conditions and situation.

DEMONSTRATES SKILLS NEEDED FOR AGE SPECIFIC CARE

MET

NOT MET

N/A

COMMENTS

Allows for possible hearing and/or vision loss, speaking in lower, louder tones as necessary; provides additional or brighter lighting, larger print for reading. Communicates all patient instructions slowly, speaking distinctly; allows time for patient to process information and respond.

Staff Member is Competent to provide Care and Services to Age Ranges Indicated. Staff Member Requires Further Education to Provide care and Services to the Age Ranges Indicated. Scheduled Date of Re-review: _______________________

Comments:

Reviewer's Signature:____________________________________ Review Date:

POLICY AND PROCEDURE MANUAL EPILEPSY MONITORING SERVICES

STANFORD HOSPITAL AND CLINICS EMU Technologists

Responsibilities 1. Will program and operate long-term epilepsy monitoring system. This includes programming of seizure and spike detection software according to laboratory parameters as well as creating appropriate montages specifically for individual patients. This is applicable to both intracranial and surface EEG recordings. 2. Must be able to recognize clinical and electrographic seizures as well as both obvious and subtle epileptiform discharges and distinguish them from artifact from both surface and intracranial recordings. 3. Print hard copy of EEG waveforms

4. Troubleshoot technical problems with computer and video equipment and repair if possible. 5. Set-up electrical stimulator and record electrical brain stimulation for brain-mapping. 6. Perform intra-operative electrocorticography (ECOG) and language mapping during epilepsy surgery. 7. Maintain proper iris, zoom, and focus of each patient's video camera. 8. 9. Archive video seizure recordings onto storage media. Organize, clean, and maintain all equipment and supplies.

10. Measuring and apply surface electrodes utilizing the international 10-20 system of electrode placement using both collodion and paste as needed. Secure and protect recording electrodes with Kling gauze and Coflex wrap according to unit protocols. 11. Produce recordings utilizing up to 128 electrode contacts and correctly connect to recording equipment, create new input protocols

and display montages, and select pertinent contacts for seizure detection. 12. Be familiar with sterile technique. Set-up and assist nursing staff with sterile dressing change for intracranial patients. 13. Maintain integrity of recording electrodes by adding conductive gel when needed and replacing when necessary. 14. Interact with patients during their clinical seizures according to established safety protocols to determine changes in level of consciousness. 15. Tech Ills will assist in teaching and supervising the work of less experienced Tech I & IIs 16. Maintain proper use and storage of volatile chemicals (collodion and acetone) and participate in air quality studies. 17. Will interact daily with nursing, ancillary staff, and physicians of all levels.

EPILEPSY MONITORING UNIT PROFICIENCY STANDARDS ELECTRODE APPLICATION --color coded correctly -sphenoidals correct --EKG applied -proficient head wrapping technique ELECTRODE APPLICATION Ph.II (2 techs required) --correct surface electrodes -ribbon cables correctly labeled and doublechecked -patient cables labeled/numbered -ability to setup/order supplies for dressing change --proficient at sterile dressing change including assessing wound site and frequency of dressing change schedule preamplifier -inputs properly selected -additional electrodes/monitors properly labeled and noted preamplifier(2 techs required) -inputs properly selected --each preamplifier labeled/numbered --additional electrodes/monitors properly labeled and noted -proper linkage between "jumpers" -appropriate patient cable connected to Digiplex --wrap preamplifiers prior to placing into "fanny pack" COMPUTERS SETUP/PROGRAM EEG MACHINE routine EEG long-term monitoring video-EEG ambulatory EEG Intraoperative corticography TAPE LABELING --patient ID impression --correct numbering -correct date --issue logsheet for new patient as needed PATIENT --demonstrate ability to assess appropriate time to hook patient up (flexible) -thoroughly explain procedure, pushbulb, dayroom, etc. --;ive icgsne.et and explain -safety issues (pads in place); Ph.11-posey/bathroom instructions SCANNING EVENT DETECTORS -accurately recognizes events --consistently notes event times

--save file until events are verified

PLAYBACK Ph.l

-adequate lead-in time --adequate clinical notations -labeled properly -timescribe functioning and correct --appropriate days printed

PLAYBACK Ph.II

- a d e q u a t e l e a d - i n t i m e -adequate clinical notations -labeled properly --timescribe functioning and correct -common channel included - ability to program any changes requested (computer & EEG instrument)

MASTERING

-accurate ly que -up eve nt (1 mi nut e lea d-in ) --appropriate digital copies- c o r r e c t M R * e s t a b l i s h e d -no more than 10 patients per tape - a d d i t i o n a l b a c k u p c o py m a d e --no original tapes of events erased until master/backup tapes checked -accurately log-in information to Master Log

TROUBLESHOOTING
-no EEG data -no video -60Hz -electrode artifact -cable problems (encoder box, patient cable, ribbon cable, etc.) --transferring from patient room to dayroom back to patient room -computer failures (beeping, log-on problems, etc.) -acquisition recorder error messages

POLICY AND PROCEDURE MANUAL NEURODIAGNOSTIC LABS

OVERTIME HOURS POLICIES

1. The utilization of overtime hours by lab personnel will be necessary at times to extend the services of the Neurodiagnostic Labs beyond the standard scheduled hours of operation to meet the needs of the patient workload. It may be required that staff work hours over their regularly scheduled time to provide lab testing procedures to maintain a high standard and continuum of patient care. 2. All overtime must be evaluated and approved by the manager of the labs. The manager will determine the personnel to fill the overtime requirements.

3. Overtime hours will be recorded outside of the standard staffing hours of operation of the Neurodiagnostic Labs: Monday to Friday, 07:00 to 17:00 hrs. 4. CALL BACK TIME: It is the policy of the Neurodiagnostics Labs to provide emergency testing procedures for SUH and LPCH from 17:00 to 07:00 hrs weekdays and 24 hours a day on weekends through technologists on-call. Call back time will be treated as overtime hours if they exceed the regular hours for an employee. Studies requested on-call must be approved by the attending neurologist or the electroencephalographer on-call before it can be performed. 5. WEEKEND EPILEPSY COVERAGE: The Epilepsy Monitoring Unit functions to monitor epilepsy patients on a 24-hour basis. When patient monitoring extends into the weekend technologists are scheduled on a rotating basis to perform routine duties that must be carried out daily (e.g. check quality of recording, rewrap patients, print hardcopy of seizures for physician interpretation, etc). Weekend hours will be treated as overtime hours if they exceed the regular hours for an employee.

STANFORD UNIVERSITY MEDICAL CENTER

DEPARTMENT OF NEUROLOGY AND NEUROLOGICAL SCIENCES STANFORD, CALIFORNIA 94305-5235 FAX (415) 725-7459

SEDATION DURING INSERTION OF SPHENOIDAL ELECTRODES PROTOCOL I. Purpose

For those patients who have excessive anxiety regarding insertion of sphenoidal electrodes or in whom the physician feels that sedation and pain control may make insertion more tolerable to the patient, the following medications may be administered according to the doses listed below. II. Procedure These medications should only be administered by a physician, preferably with an RN in attendance. All medications are administered intravenously. A) Midazolam 0.4mg/kg (2mg for an average size adult). The Midazolam should be given in two doses separated by 5 minutes, i.e. lmg in each dose. B) Meperidine 1.4mg/kg (60mg for an average size adult). The Meperidine should be given in two doses separated by 5 minutes, i.e. 30mg in each dose. C) I.V. normal saline should be available as well as an ambu-bag and Naloxone 1 amp, drawn up in a syringe by bedside. Blood pressure should be checked prior to administration of the medications and after each of the two doses. The patient should be observed for at least 10 minutes following the final dose.

D) E)

Approved by: Martha Morrell, M.D. Original date: 3/1/91 Re-aaproved by Robert S. Fisher, MD, PhD 7/26/2010

Stanford University Hospital EEG/Epilepsy Procedures for the Use of Collodian

1.0 PURPOSE This section was developed to aid Stanford University Hospital with regards to employee and patient exposure to collodian, specifically Ethyl Ether. EEG electrode application, utilizing collodian as the adhesive to a patient's scalp, invariably releases fumes into the room air. Occupational exposure to such fumes above certain levels may be hazardous to the health of exposed personnel, therefore the concentration levels present in the room should not exceed the Permissible Exposure Limit (PEL) 2.0 REFERENCE 2.1 California Code of Regulations Title 8 Section 5155 3.0 PROCEDURES

Electroencephalogram Department
The application of EEG electrodes with the use of collodian is routinely performed on the inpatient F3 unit for video/EEG evaluation in the Epilepsy Monitoring patient rooms (Room. #336, 339, 341, 342, and the Dayroom #338). Occasionally collodian application is performed in the EEG Laboratory (Room. #3132D and H3132E). The method utilized to affix the EEG electrodes to the patient's scalp is to saturate a small gauze patch with collodian, place the gauze over the scalp electrode, and dry the patch with an air compressor This procedure is repeated for each electrode site (approximately 25) and is completed within 20 to 30 minutes. 4.0 RESPONSIBILITIES 4.1 Environmental Health and Safety Department The Environmental Health and Safety Department (EH/S) is responsible for performing air monitoring tests for Ethyl Ether and documenting that the employees working with Ethyl Ether are monitored to ensure that they are not exposed above the Permissible Exposure Limit.

4.2 Department Managers and Supervisors

Department Managers and Supervisors are responsible to implement the exposure control program to keep daily chemical exposure in a state of control below the Permissible Exposure Limit.

5.0 AIR MONITORING METHODS 5.1 A personal air monitoring badge is used to sample Ethyl Ether for 8 hour Time Weighted Average (TWA). The Permissible Exposure Limit for Ethyl Ether is 400 parts contaminant per million parts of air over TWA.
5.2 The Miran 1B2 is used to conduct air sampling for Ethyl Ether on a Short Term Excursion Limit (STEL) for 15 minutes. The Permissible Exposure Limit for Ethyl Ether is 500 parts contaminant per million parts of air over STEL.

6.0 REPORTING
The results of all tests are provided to the affected employees and reported to the Employee Health Department, Environmental Health and Safety Department, and Hospital Safety Committee.

7. 0 MEDICAL SURVEILLANCE
Initial personnel monitoring will be from the breathing zone air samples that are representative of the 8 hour TWA exposure of each employee, using an applicable monitoring badge. STEL sampling will be done by monitoring work activities using the air sampling equipment.

ENVIRONMENTAL HEALTH & SAFET

Date: To: From: Subject:

I.

April 3, 1998 Mark Burde11, Manager Neurodiagnostics Department Jeffrey Narita, Industrial Hygienist Environmental Health and Safety Department Personal Air Monitoring for Ethyl Ether

300 Pasteur Drive. Room FEGOO Stanford, CA 94305

Tel. 650.723.8143 Fax 650.725.4633

On March 23, 1998 personal air monitoring for ethyl ether was conducted in room HF341 and 1-1F336. The purpose of the monitoring was to measure Ms. Diep Phan EEG technician, personal exposure to ethyl ether during her routine procedures. Passive personal air monitoring measurements for a 15-minute short term exposure limit (STEL) and 8hour Time Weighted Average (TWA) was performed to evaluate for compliance with the California Occupational Safety Health and Administration (Cal/OSHA) ethyl ether permissible exposure limit (PEL). The California Code of Regulations, General Industry Orders, Title 8 Section 5155 sets a standard for ethyl ether of 500 parts per million (ppm) as a STEL concentration and 400 ppm as a TWA. Personal air sampling was conducted to determine the exposure to ethyl ether. Breathing zone measurements were collected while Ms. Diep Pham performed her regular duties which involves applying electrodes on patients scalp using cons-ugh which rnntains ethyl ether, This is done with dipping a gauze like tape into a one inch cup of collodian and taping the electrodes for adhesive purposes. An air compressor was used to expedite the drying process.
Passive Badges

Purpose

II. Standard

III. Personal Air Sampling Methodology

Dinitrophenol hydrazine, passive air monitoring badges by ChemExpress were used and then sent to Assay Technology of Palo Alto for analysis. Assay Technology Lab is accredited by the American Industrial Hygiene Association. The number in the exposure column describes the minimum level of detection of ethyl ether in ppm of air. As the Cal/OSHA STEL is 500 ppm of air over a 15-minute time period and TWA is 400 ppm over a 8-hour time period. The results indicates the concentration of ethyl ether in air is well below the Cal/OSHA PEL. Time Exposure Badge ID Sample Date h rs. ppm BN3238 BN3198 3N3315
V. Recommendation IV. Air Sampling Results

3/23/98 3/23/98 3/23/98

N/A .25 7.42

Control 130 ppm (STEL) 18 ppm (TWA)

Based on the personal air sample results, measurement level was well below the Cal/OSHA PEL's. If you have any questions regarding this report, please call me at 3-8143 or email me at Narita). Thank you.

e+

%A. technology

assay

The Technology Leader in Personal Monitoring for Chemicals in the Workplace

AM A- Accredited 01124

LABORATORY ANALYSIS REPORT

Received: March 25, 1998 To: Analyzed: March 30, 1998 Mr Jeff Narita Stanford Hospital 300 Pasteur Dr HG001 Stanford, CA 94305

Your air sample has been analyzed and the results are reported as Total Exposure in ppm-hours. If sampling times have been provided, the Time-Weighted-Average Exposure Level, and the associated Detection Limit, in ppm have also been calculated.
Exposure Level (ppm) = Total Exposure (ppm-hrs) I Time (hrs)
Ref Badge Name / Area I D Monitored Sample Date 3/23/98 Substance Monitored Ethyl Ether Total Exp Time Exposure Det Limit ppm-hrs hrs ppm ppm 136. 7.42 18. 0.081

98-7084 12C97 Diep Pham 6N3315

NOTES:
Method AT541: Modified 'OSHA V, Media: Charcoal, Analysis: GC/FiD

If you have questions about this report, please contact us no later than April 29, 1998.

Analyst: Ahmed R. Orgunwall Results Approved by

Date Format: Month/Day/Year

Signoff _______________________________________________________________________ Initials / Date

aassay technology

The Technology Leader in Personal Monitoring for Chemicals in the Workplace

AMA-Aceredikod *11124

LABORATORY ANALYSIS REPORT

Received: March 25, 1998 To: Analyzed: March 30, 1998 Mr Jeff Narita Stanford Hospital 300 Pasteur Dr HG001 Stanford, CA 94305

Your air sample has been analyzed and the results are reported as Total Exposure in ppm-hours. If sampling times have been provided, the Time-Weighted-Average Exposure Level, and the associated Detection Limit, in ppm have also been calculated.

Exposure Level (ppm) = Total Exposure (ppm-hrs) / Time (hrs)

Sample Date Ref Badge Name / Area I D Monitored 3/23/98 Substance Monitored Ethyl Ether Total Exp ppm-hrs 32.3 Time Exposure Det Limit ppm 2.4

hrs ppm .25 130.

NOTES: Method AT541: Modified ( - )! - !.4 #7, Media: rharcoal, Analysis: OCIF1,0 If you have questions about this report, please contact us no later than April 29, 1998.

Analyst Ahmed R. Orgunwall

Date Format Month/Day/Year

Results Approved by

Signoff ______________________________________________________________________ Initials / Date

MATERIAL SAFETY DATA SHEET

Manufacturer: Mavidon Corporation 3953 SW Bruner Terrace Palm City, FL 34990 Date Prepared: 12/92 Emergency Phone Number: (407) 286-8951 or (800) 535-5053

SECTION 1 - GENERAL INFORMATION IDENTITY ...: Mavidon COLLODION, REGULAR SECTION II - HAZARDOUS INGREDIENTS/SARA III INFORMATION

TRADE NAIVE,CHEMICAL NAME

OCCUPATIONAL TLV/PEL/STEL

VAPOR PRESSURE MM Hg @TBAPERAMRE

PERCENT

Cellulose Nitrate (CAS # 9004-70-0) N/A Ethanol (CAS 4 64-17-5) 1000 ppm Ethyl Ether (CAS 4 60-29-7) 70

N/A 5 47.0 @ 68F 25 400 ppm442.0 @ 68 aF

**0 No toxic chemical(s) subject to the reporting requirements of section 313

of title III and of 40 CFR 372 are present. lb" All components contained in this product are TSCA registered**** DOT Description: Nitrocellulose, Solution, Flammable UN2059 HMIS: Aealtn - 2 Flammability - 4 Reactivity - 2 Personal Prot. - D

Reports have associated repeated and prolonged occupational overexposure to solvents with permanent brain and nervous system damage. Intentional misuse by deliberately concentrating and inhaling the content:. may be harmful or fatal.

SECTION III - PHYSICAL DATA Boiling Point (0F) ......... 96,0000 Specific Gravity: . (H20 = 1)..: 0.8 Vapor Pressure (mm/Hg) .... NA Vapor Density (Air = 1) .... Heavier Melting Point ............. NA Evaporation Rate ........... Slower than ether Coating V.0 C ............... ' 5.99 lb/g1 (718 g/l) Material V.0 C ............. 5.99 'big' (718 g/1) Solubility in Water ........ Slight Appea rance & Odor ................ Ether/Alcohol

SECTION IV - FIRE & EXPLOSION HAZARD DATA F lash Point (T.O.C.) ...... -490F (T.C.C.) Flammable Limits ............ L.E.L.: 1.9% U.E.L.: 36.0% Extinguishing Media .......... Extinguish fires with foam, alcohol foam,CO2 dry chemicals, water fog. Special Fire Fighting Procedures: Do not enter fire space without prope protective equipment, including a NIOSH approved self-contained breathin apparatus. Keep containers in storage cool with water to prevent pressur build up and bursting. Unusual Fire & Explosion Hazards: Dry nitrocellulose resin is extremel flammable and burns explosively. Avoid friction and impact to any quantit of dry resin. Burning rate increases with quantity and confinement. *Product contains ethyl ether, extremely flammable*. Toxic degradatio products include: Oxides of nitrogen, carbon dioxide, carbon monoxide, dens toxic smoke is formed when material burns. SECTION V - REACTIVITY DATA STABILITY: Stable CONDITIONS TO AVOID: Heats, sparks, flames and Avoid allowing unmodified resin to become dry. INCOMPATIBILITY (MATZRIAL3 70 AVOID): 'Strong amines. HAZARDOUS DECOMPOSITION CR BYPRODUCTS: Oxides of carbon dioxide and other toxic asses. HAZARDOUS POLYMERIZATION: Vitt not occur.

other sources of ignition. Avoid friction and impact. oxidizers, acids, bases ar nitrogen, carbon monoxide

SECTION VI - HEALTH HAZARD DATA

INHALATION HEALTH RISKS AND SYMPTOMS OF EXPOSURE: Headache, lethargy, drowsiness, weakness, difficulty walking, personality change, poor appetite, rash and weight loss. Prolonged exposure to vapors in concentrations in excess of TLV can cause damage to kidneys, blood and nervous system. SKIN AND EYE CONTACT HEALTH RISKS AND SYMPTOMS OF EXPOSURE: Liquid may cause eyes to become irritated, prolonged exposure to skin may cause drying and cracking. SKIN ABSORPTION HEALTH RISKS AND SYMPTOMS OF EXPOSURE: Prolonged absorption of material through skin could cause damage to blood, kidneys and nervous system. INGESTION HEALTH RISKS AND SYMPTOMS OF EXPOSURE: Headache, lethargy, drowsiness, weakness, difficulty walking, personality change, poor appetite, rash and weight loss. HEALTH HAZARDS (ACUTE AND CHRONIC): Vapor irritation to eyes, nose and throat. Liquid irritating to eyes and skin. Prolonged and repeated exposure to vapor concentrations in excess of TLV or through prolonged absorption through skin may cause damage to blood, kidneys and nervous system. CARCINOGENICITY: NTP: No IRAC MONOGRAPHST: No OSHA REGULATED: No

MEDICAL CONDITIONS GENERALLY AGGRAVATED BY EXPOSURE: EMERGENCY AND FIRST AID PROCEDURES: INHALATION: Remove victim to fresh air. If not breathing, give artificial respiration. Give oxygen if breathing is difficult . Get medical attention immediately. EYE OR SKIN CONTACT: Immediately flush with plenty of fresh water. Remove contaminated shoes and clothing. Get medical attention. SECTION VII - PRECAUTIONS FOR SAFE HANDLING AND USE STEPS TO BE TAKEN IN CASE OF RELEASE OR SPILL: Immediately eliminate all sources of ignition. Use appropriate absorbent. Large spills may be placed into a suitable container for disposal. TASTE DISPOSAL METHOD: Incinerate in an approved incinerator or dispose of in a chemical dump in accordance with local, state, county and federal regulations regarding health and environment. PRECAUTIONS TO BE TAKEN IN HANDLING AND STORING: Keep containers tightly closed, cool dry and away from sources of heat, sparks, and ignition.Dry nitrocellulose is extremely flammable. Use with adequate ventilation. OTHER. PRECAUTIONS: Use only non-sparking tools. Ground all containers before transferring material.

COLLODION, REGULAR Page 4 SECTION VIII - CONTROL MEASURES RESPIRATORY PROTECTION: Supplied air respiratory protection for large spills or confined spaces. VENTILATION: Mechanical or supplemental local exhaust may be required to keep vapor concentrations below TLV. PROTECTIVE GLOVES, EYEWARE, ETC.: Plastic or rubber gloves, safety glasses with side shields, rubber apron, safety shoes. Sufficient clothing to prevent

contact with skin. Wash thoroughly after handling. SECTION IX - DISCLAIMER To the best of our knowledge the above statement are true, we cannot anticipate every condition of use, or control how our product is handled outside our plant. Therefore, the above statements do not express or imply any warranty, or guarantee of accuracy or applicability. Please consult local, state and federal agencies for current regulatory status of material.

NE - none established

NA - not applicable ND - none determined

J. T. BAKER CHEMICAL CO. 222 RED SCHOOL LANE, PHILLIPSBURG, NJ 08865 M A T E R I A L S A F E T Y D A T A S H E E T 24-HOUR EMERGENCY TELEPHONE -- (201) 859-2151 CHEMTREC 4 (800) 424-9300 -- NATIONAL RESPONSE CENTER t (800) 424-8802 A0446 -01 EFFECTIVE: 10/11/85 SECTION I PRODUCT IDENTIFICATION

ACETONE

PAGE: ISSUED: 01/23/8

58.08 CAS NO.: 00067-64-1 NIOSH/RTECS NO.: AL3150000

PRODUCT NAME: FORMULA: FORMULA WT:

ACETONE

(CH3)2C0

COMMON SYNONYMS: DIMETHYL KETONE; METHYL KETONE; 2-PROPANONE PRODUCT CODES:

9010,9006,9002,9254,9009,9001,9004,5356,A134,9007,9005,9008 PRECAUTIONARY LABELLING BAKER SAF-T-DATA(TM) SYSTEM HEALTH FLAMMABILITY - 3 (FLAMMABLE) REACTIVITY CONTACT - 1 LABORATORY PROTECTIVE EQUIPMENT SAFETY GLASSES; LAB COAT; VENT HOOD; PROPER GLOVES; CLASS B EXTINGUISHER PRECAUTIONARY LABEL STATEMENTS DANGER EXTREMELY FLAMMABLE HARMFUL IF SWALLOWED OR INHALED CAUSES IRRITATION KEEP AWAY FROM HEAT, SPARKS, FLAME. AVOID CONTACT WITH EYES, SKIN, CLOTHING. AVOID BREATHING VAPOR. KEEP IN TIGHTLY CLOSED CONTAINER. USE WITH ADEQUATE VENTILATION. WASH THOROUGHLY AFTER HANDLING. IN CASE OF FIRE, USE WATER SPRAY ALCOHOL FOAM, DRY CHEMICAL, OR CARBON DIOXIDE. FLUSH SPILL AREA WITH WATER SPRAY. SECTION II -- HAZARDOUS COMPONENTS
-

COMPONENT ACETONE SECTION III PHYSICAL DATA BOILING MELTiNG POINT: 56 C 133 F) VAPOR PRESSUREYMM HG) 1S1 VAPOR DENSITYKAIR=1): EVAPORATION RATE: 5. 6 (BUTYL ACETATE=1) CONTINUED ON PAGE: 2 90-100

=25 C ( 13? F)

SPECIFIC GRAVITY: 0.79 (H20:=1)

J. T. BAKER CHEMICAL CO. 222 RED SCHOOL LANE, PHILLIPSBURG, NJ 08865 MATERIAL SAFETY DATA SHEET 24--HOUR EMERGENCY TELEPHONE -- (201) 859-2151 CHEMTREC t (800) 4249300 -- NATIONAL RESPONSE CENTER 4 (800) 424-8802 A0446 --01 EFFECTIVE: 0/11/85 ACETONE PAGE: ISSUED: 01/23/8e

SECTION III PHYSICAL DATA (CONTINUED)SOLUBILITY(H20): COMPLETE (IN ALL PROPORTIONS) Z VOLATILES BY VOLUME: 100 APPEARANCE & ODOR: CLEAR, COLORLESS LIQUID WITH FRAGRANT SWEET ODOR. SECTION IV FIRE AND EXPLOSION HAZARD DATA FLASH POINT: 18 C 0 F) NFPA 704M RATING: 1-3-0 FLAMMABLE LIMITS: UPPER 13 % LOWER 2 %

FIRE EXTINGUISHING MEDIA USE ALCOHOL FOAM, DRY CHEMICAL OR CARBON DIOXIDE. (WATER MAY BE INEFFECTIVE.) SPECIAL FIREFIGHTING PROCEDURES FIREFIGHTERS SHOULD WEAR PROPER PROTECTIVE EQUIPMENT AND SELFCONTAINED (POSITIVE PRESSURE IF AVAILABLE) BREATHING APPARATUS WITH FULL FACEPIECE. MOVE EXPOSED CONTAINERS FROM FIRE AREA IF IT CAN BE DONE WITHOUT RISK. USE WATER TO KEEP FIREEXPOSED CONTAINERS COOL. UNUSUAL FIRE & EXPLOSION HAZARDS VAPORS MAY FLOW ALONG SURFACES TO DISTANT IGNITION SOURCES AND FLASH RACK CLOSED CONTAINERS EXPOSED TO HEAT MAY EXPLODE. CONTACT WITH STRONG OXIDIZERS MAY CAUSE FIRE. SECTION V -- HEALTH HAZARD DATA THRESHOLD LIMIT VALUE TLV/TWA): 1780 MG/M3 ( 750 PPM)

SHORT--TERM EXPOSURE LIMIT (STEL): 2375 MG/M3 ( 1000 PPM) TOXICITY: LD50 (ORALRAT)(MG/KG) LD50 (IPRMOUSE)(G/KG) 9750 1297

EFFECTS OF OVEREXPOSURE CONTACT WITH SKIN HAS A DEFATTING EFFECT, CAUSING DRYING AND IRRITATION. OVEREXPOSURE TO VAPORS MAY CAUSE IRRITATION OF MUCOUS MEMBRANES, DRYNESS OF MOUTH AND THROAT, HEADACHE, NAUSEA AND DIZZINESS. EMERGENCY AND FIRST AID PROCEDURES CALL A PHYSICIAN. IE SWALLOWED, 1;r CONSCIOUS, flINEDIATELY INDUCE VOMITING. IF INHALED, kiLNOVE TO FRESH AIR. IF NOT BREATHING, GIVE ARTIFICIAL RESPIRATION. IE BREATHING IS DIFFICULT, GIVE OXYGEN. IN CASE OF CONWiCT, IMMEDIATELY FLUSH EYES WITH PLENTY OF WATER FOR AT LEAST 15 MINUTES. FLUSH SKIN WITH WATER. CONTINUED ON PAGE: 3

J. T. BAKER CHEMICAL CO. 222 RED SCHOOL LANE, PHILLIPSBURG, NJ 08865 MATERIAL SAFETY DATA SHEET 24-HOUR EMERGENCY TELEPHONE -- (201) 859-2151 CHEMTREC t (800) 424--9300 -- NATIONAL RESPONSE CENTER t (800) 4248802 A0446 -Of ACETONE PAGE: EFFECTIVE: 10/11/85 ISSUED: 01/23/8 -------------- - - ------------------------------------------------SECTION VI - REACTIVITY DATA STABILITY: STABLE CONDITIONS TO AVOID: HAZARDOUS POLYMERIZATION: WILL NOT OCCUR HEAT, FLAME, SOURCES OF IGNITION

INCOMPATIBLES:

SULFURIC ACID, NITRIC ACID, STRONG OXIDIZING AGENTS SECTION VII - SPILL AND DISPOSAL PROCEDURES

STEPS TO BE TAKEN IN THE EVENT OF A SPILL OR DISCHARGE WEAR SUITABLE PROTECTIVE CLOTHING. SHUT OFF IGNITION SOURCES; NO FLARES, SMOKING, OR FLAMES IN AREA. STOP LEAK IF YOU CAN DO SO WITHOUT RISK. USE WATER SPRAY TO REDUCE VAPORS. TAKE UP WITH SAND OR OTHER NON-COMBUSTIBLE ABSORBENT MATERIAL AND PLACE INTO CONTAINER FOR LATER DISPOSAL. FLUSH AREA WITH WATER. J. T. BAKER SULUSORB(R) SOLVENT ADSORBENT IS RECOMMENDED FOR SPILLS OF THIS PRODUCT. DISPOSAL PROCEDURE DISPOSE IN ACCORDANCE WITH ALL APPLICABLE FEDERAL, STATE, AN!) LOCAL ENVIRONMENTAL REGULATIONS. EPA HAZARDOUS WASTE NUMBER: U002 (TOXIC WASTE) ---------- _ - -------------------' SECTION VIII - PROTECTIVE EQUIPMENT VENTILATION: USE GENERAL OR LOCAL EXHAUST VENTILATION TO MEET TLV REQUIREMENTS.

RESPIRATORY PROTECTION: RESPIRATORY PROTECTION REQUIRED IF AIRBORNE CONCENTRATION EXCEEDS TLV. AT CONCENTRATIONS UP TO 5000 PPM, A GAS MASK WITH ORGANIC VAPOR CANNISTER IS RECOMMENDED. ABOVE THIS LEVEL, A SELF-CONTAINED BREATHING APPARATUS WITH FULL FACE SHIELD IS ADVISED. EYE/SKIN PROTECTION: SAFETY GLASSES WITH SIDESHIELDS, POLYVINYL ACETATE GLOVES ARE RECOMMENDED.

SECTION IX - STORAGE AND HANDLING PRECAUTIONS !::AF-T-DATA(TM) STORAGE COLOR CODE: RED

SPECIAL PRECAUTIONS BOND AND GROUND CONTAINERS WHEN TRANSFERRING LIQUID. KEEP CONTAINER TIGHTLY CLOSED. STORE IN A COOL, DRY, WELL-VENTILATED, FLAMMABLE LIQUID STORAGE AREA. CONTINUED ON PAGE : 4

J. T. BAKER CHEMICAL CO. 222 RED SCHOOL LANE, PHILLIPSBURG, NJ 08865 MATERIAL SAFETY DATA SHEET 24-HOUR EMERGENCY TELEPHONE --- (201) 859-2151 CHEMTREC t (800) 424-9300 -- NATIONAL RESPONSE CENTER * (800) 424-8802 A0446 -01 EFFECTIVE: 10/11/85 ACETONE PAGE: -= ISSUED: 01/23/8,!

SECTION X - TRANSPORTATION DATA AND ADDITIONAL INFORMATION DOMESTIC (D.O.T.) PROPER SHIPPING NAME HAZARD CLASS UN/NA LABELS INTERNATIONAL (I.M.O.) PROPER SHIPPING NAME HAZARD CLASS UN/NA LABELS ACETONE FLAMMABLE LIQUID UNi090 FLAMMABLE LIQUID

ACETONE 3.1 UNi090 FLAMMABLE LIQUID

(TM) AND (R) DESIGNATE TRADEMARKS. N/A = NOT APPLICABLE OR NOT AVAILABLE --THE INFORMATION PUBLISHED IN THIS MATERIAL SAFETY DATA SHEET HAS BEEN COMPILED =ROM OUR EXPERIENCE AND DATA PRESENTED IN VARIOUS TECHNICAL PUBLICATIONS. IT I. THE USER'S RESPONSIBILITY TO DETERMINE THE SUITABILITY OF THIS INFORMATION FOR THE ADOPTION OF NECESSARY SAFETY PRECAUTIONS. WE RESERVE THE RIGHT TO REVISE AS NEW INFORMATION BECOMES AVAILABLE.-- LAST PAGE --

MATERIAL SAFETY DATA SHEET

PRODUCT NAME: COLLODION H V
GENERAL USE: Medical Skin Coating PRODUCT DESCRIPTION: Extremely flammable clear liquid, ether odor
N II a NI `

SECTION 1- PRODUCT AND COMPANY IDENTIFICATION

aon

M A N UF AC TUR ER 'S NA ME Mavidon Medical Products ADDRESS (NUMBER, STREET, P.O. BOX) 2105 7th Avenue North (CITY, STATE AND ZIP CODE) Lake Worth, FL 33461DISTRIBUTOR'S NAME Same ADDRESS (NUMBER, STREET, P.O. BOX) (CITY, STATE AND ZIP CODE)

COUNTRY USA

DATE PREPARED: July 29, 2001 Page 1 of 4 SUPERSEDES: New TELEPHONE NUMBER FOR INFORMATION (561) 585-2227 EMERGENCY TELEPHONE NUMBER Infotrac 800) 535-5053 Outside USA (352) 323-3500

TEL E P H ON E N U MB ER F O R I N FOR M ATI O N COUNTRY EMERGENCY TELEPHONE NUMBER

SECTION 2 - HAZARDOUS INGREDIENTS

HAZARDOUS COMPONENTS Ethyl ether (a,b) Ethanol Nitrocellubse, colloided, granular CAS #
(by weight)

OS H A P E L
ppm MG/M3

ACGIH TWA
PPM MG/M3

SARA
TITLE III

RQ
LBS

60-29-7 64-17-5 9004-70-0

60 - 70 20 - 30 5- 10

400 1000

1200 1900

400 1000

100

not established

(a) See Section 15

(b) Indicates that the Resource Conservation and Recovery Act (RCRA) has determined the waste for this chemical is listed as hazardous and must be handled according to regulations in 40 CFR 260-281.

SECTION 3 - HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW
Clear amber extremely flammable viscous liquid, potentially hazardous vapors. vapors can cause anesthetic effect leading to death in poorly ventilated areas Can cause eye and skin irritation upon contact. Inhalation of Hazard symbols for this product - F, XI. XN

POTENTIAL HEALTH EFFECTS

INHALATION: Inhalation of mists or vapors may cause irritation to upper respiratory tract and mucous membranes.

SKIN: Skin irritant, contact with the skin will cause irritation, local redness.

EYES: This product is an eye irritant. Contact with the eyes will cause irritation.

INGESTION: May cause gastric distress, vomiting and diarrhea.

CARCINOGENICITY

NIP?

No

IARC MONOGRAPHS?

No

OSHA REGULATED?

No

MATERIAL SAFETY DATA SHEET

PRODUCT NAME: COLLODION H V July 29, 2001 Page 2 of 4

SECTION 4 - FIRST AID MEASURES

INHALATION: Remove affected person to fresh air; if symptoms persist seek medical attention.

SKIN: Remove contaminated clothing; wash affected area with soap and water; launder contaminated clothing before reuse: if irritation persists, seek medical attention. EYES: Remove contact lenses. Flush eyes with clear running water for 15 minutes while holding eyelids open; if irritation persists, seek medical attention. INGESTION: Give two glasses of water for dilution; DO NOT induce vomiting; seek medical attention; never give anything by mouth to an unconscious person.

SECTION 5 - FIRE FIGHTING MEASURES

F L AS H P OI NT (M E T H OD US ED) -32 F ( -35.5 C) TCC FLAMMABLE LIMITS LEL: 1 9% UEL: 36.0%
IA

AUTOIGNITION TEMPERATURE: Not determined i NFPA CLASS: GENERAL HAZARDS: Product is extremely flammable. Products of combustion include compounds of carbon, hydrogen and oxygen, including carbon monoxide. Vapors may cause a flash fire or ignite explosively. Vapors may travel a considerable distance to a source of ignition and flash back. EXTINGUISHING MEDIA Carbon dioxide, water fog, dry chemical, chemical foam FIRE FIGHTING PROCEDURES Firefighters must wear full facepiece self - contained breathing apparatus in positive pressure mode. Do not use solid stream of water since stream will scatter and spread fire. Fine water spray can be used to keep fire - exposed containers cool. UNUSUAL FIRE AND EXPLOSION HAZARDS Closed containers can explode due to buildup of pressure when exposed to extreme heat. Do not use direct stream of water on pool fires as product may reignite on water surface. Caution - Material is extremely flammable! HAZARDOUS COMBUSTION PRODUCTS Smoke, fumes, oxides of carbon

SECTION 6 - ENVIRONMENTAL RELEASE MEASURES

STEPS TO BE TAKEN IN CASE MATERIAL IS RELEASED OR SPILLED CAUTION - EXTREMELY FLAMMABLE - Evacuate and ventilate area; confine and absorb into absorbent; place material into approved containers for disposal; for spills in excess of allowable limits (RQ) notify the National Response Center (800) 424 - 8802; refer to CERCLA 40 CFR 302 for detailed instructions concerning reporting requirements.

SECTION 7-HANDLING AND STORAGE

PRECAUTIONS TO BE TAKEN IN HANDLING AND STORAGE: Keep container closed when not in use; protect containers from abuse; protect from extreme temperatures. CAUTION - EXTREMELY FLAMMABLE - keep away from all sources of ignition. "Empty" containers may contain residue which may form explosive vapors. Do not weld or cut near empty container that has not been professionally reconditioned. Use non-sparking tools when opening and closing containers. Maintain well ventilated work areas to minimize exposure when handling this material.

SECTION 8 - EXPOSURE CONTROLS / PERSONAL PROTECTION

ENGINEERING CONTROLS The use of local exhaust ventilation is recommended to control emissions near the source. Provide mechanical ventilation of confined spaces. Use explosion-proof ventilation equipment. See Section 2 for Component Exposure Guidelines. PERSONAL PROTECTION: RESPIRATORY PROTECTION (SPECIFY TYPE): None required: however, if misting occurs, NIOSH approved respirator capable of removing particulate from air must be worn. Refer to 29 CFR 1910.134 or European Standard EN 149 for complete regulations. PROTECTIVE GLOVES: Neoprene or rubber gloves with cuffs. EYE PROTECTION: Safety goggles with side shields OTHER PROTECTIVE CLOTHING OR EQUIPMENT: Safety eyebath nearby WORK / HYGIENIC PRACTICES: Practice safe workplace habits. Minimize body contact with this, as well as all chemicals in general.

MATERIAL SAFET Y DATA SH EET

P R O29, DUC T NAME: COLLODION H V July 2001 P a g VAPOR PRESSURE (MM Hg) 442 mm Flq @ 20 C SPECIFIC GRAVITY (WATER = 1) 0.805 SOLUBILITY IN WATER Insoluble pH Not determined BOILING POINT 94 F (34.4 C) VISCOSITY Not determined
STABILITY INCOMPATIBILITY (MATERIALS TO AVOID): UNSTABLE: STABLE: XXX

SECTION 9 - PHYSICAL AND CHEMICAL PROPERTIES

VAPOR DENSITY (AIR = 1) >1 EVAPORATION RATE (WATER = 1) <1 FREEZING POINT Not determined APPEARANCE AND ODOR Viscous colorless liquid, ether odor PHYSICAL STATE Liquid VOLATILE ORGANIC COMPOUNDS (Total VOC's) 6.16 lbs / gallon

SECTION 10 - STABILITY AND REACTIVITY

CONDITIONS TO AVOID: Material may form dangerous peroxides upon exposure to sunlight and air.

Strong oxidizers, strong acids HAZARDOUS DECOMPOSITION OR BYPRODUCTS: Decomposition will not occur if handled and stored properly. In case of a fire, oxides of carbon, hydrocarbons, fumes, and smoke may be produced.
HAZARDOUS P OLYMERIZAT ION MAY OCCUR: WILL NOT OCCUR: XXX CONDITIONS TO AVOID: None

SECTION 11- TOXICOLOGICAL INFORMATION

Hazardous Ingredients Ethyl ether (a,b) Ethanol Nitrocellulose, colloided, granular % 60 - 70 20 - 30 5 - 10 CAS it
LD50 of Ingredient (Specify Species and Route) 1215 mg / kg 60-29-7 Oral - rat 6 5 0 0 p p m / 9 9 M 3450 mg / kg 64-17-5 Oral - mouse LC50 of Ingredient (Specify Species)

Inhalation - mouse 20,000 ppm / 10H Inhalation - rat

9004-70-0

N o t

> 5000 mg / kg Oral - rat e s t a b l i s h e d

SECTION 12 - ECOLOGICAL INFORMATION

No data are available on the adverse effects of this material on the environment. Neither COD nor BOD data are available. Based on the chemical composition of this product it is assumed that the mixture can be treated in an acclimatized biological waste treatment plant system in limited quantities. However, such treatment should be evaluated and approved for each specific biological system. None of the ingredients in this mixture are classified as a Marine Pollutant.

SECTION 13 - DISPOSAL CONSIDERATIONS

WASTE DISPOSAL METHOD: Dispose of in accordance with Local, State, and Federal Regulations. This product may produce concentrated hazardous vapors or fumes in a disposal container creating a dangerous environment. Refer to "40 CFR Protection of Environment Parts 260 299" for complete waste disposal regulations for ignitable materials. Consult your local, state, or Federal Environmental Protection Agency before disposing of any chemicals. Do not flush to sanitary sewer or waterway.

SECTION 14 - TRANSPORT INFORMATION

PROPER SHIPPING NAME: Ethyl ether mixture

HAZARD CLASS / Pack Group: 3 / I REFERENCE: 49 CFR 173.150..201..243 IDENTIFICATION NUMBER: UN 1155 LABEL: FLAMMABLE LIQUID

IATA HAZARD CLASS / Pack Group: 3 / I IMDG HAZARD CLASS: 3 / I RID/ADR Dangerous Goods Code: 3 (2A) Canadian TDG Class / Division: 3.1 HAZARD SYMBOLS: F Note: Transportation information provided is for reference only. Client is urged to consult CFR 49 parts 100 - 177, IMDG, IATA, EC, Canadian TDG, and United Nations TDG information manuals for detailed regulations and exceptions covering specific container sizes, packaging materials and methods of shipping.

MATERIAL SAFETY DATA SHEET

PRODUCT NAME: COLLODION H V July 29, 2001 Page 4 of 4

SECTION 15 - REGULATORY INFORMATION

TSCA (Toxic substance Control Act) Components of this product are listed on the TSCA Inventory. SARA TITLE Ill (Superfund Amendments and Reauthorization Act) 311/312 Hazard Categories Acute health, flammable, skin irritant, eye irritant 313 Reportable Ingredients: None

CERCLA (Comprehensive Response Compensation and Liability Act) (a) The Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) has notification requirements for releases or spills to the environment of the Reportable Quantity (RQ for this mixture = 150 Ibs) or greater amounts, according to 40 CFR 302. CPR (Canadian Controlled Products Regulations This product has been classified in accordance with the hazard criteria of the Controlled Products Regulations and the MSDS contains all the information required by the Controlled Products Regulations IDL (Canadian Ingredient Disclosure List Components of this product listed on the Canadian Ingredient Disclosure List are shown in Section 2. EINECS (European Inventory of Existing Commercial Chemical Substances Components of this product are on the European Inventory of Existing Commercial Chemical Substances EC Risk Phrases R11 Highly flammable R20 Harmful by inhalation R36 Irritating to eyes R38 Irritating to skin. EC Safety Phrases 516 Keep away from sources of ignition S23 Do not breathe vapor 525 Avoid contact with eyes S28 After contact with skin, wash immediately with plenty of soap an S29 Do not empty into drains

SECTION 16 - OTHER INFORMATION

This product contains the following chemical substances subject to the reporting requirements of TSCA 12 (B) if exported from the United States - ethyl ether (diethyl ether)

HMIS HAZARD RATINGS

HEALTH FLAMMABILITY REACTIVITY

1 4 0 B

0 = INSIGNIFICANT 1 = SLIGHT 2 = MODERATE Safety Glasses, Gloves

3 = HIG H 4 = EXTREME

P E RSO NA L P ROTE CT IVE EQ UI PM EN T

REVISION SUMMARY:

This MSDS has been revised in the following sections: No revisions available

MSDS Prepared by:

Comprehensive Data Base Inc P.O. Box 5604 Lakeland, FL 33807 USA (863) 644 - 3298 www.compdatabase.com

The information contained herein is believed to be accurate but is not warranted to be so. Users are advised to confirm in advance of need tha information is current, applicable and suited to the circumstances of use. Vendor assumes no responsibility for Injury to vendee or third persons proximately caused by the material if reasonable safety procedures are not adhered to as stipulated in the data sheet Furthermore, vendor assumes no responsibility for injury caused by abnormal use of this material even if reasonable safety procedures are followed.

MATERIAL SAFETY DATA SHEET

PRODUCT NAME: MAVIDON LemonPrep TM
GENERAL USE: Skin Cleaner PRODUCT DESCRIPTION: Semi abrasive lotion, Citrus odor

SECTION 1- PRODUCT AND COMPANY IDENTIFICATION

M A N UF AC TUR ERS NA M E Mavidon Medical Products ADDRESS (NUMBER, STREET, P.O. BOX) 2105 7th Avenue North (CITY, STATE AND ZIP CODE) Lake Worth, FL 33461DISTRIBUTOR'S NAME Same ADDRESS (NUMBER, STREET, P.O. BOX) (CITY, STATE AND ZIP CODE)

COUNTRY USA

DATE PREPARED: October 29, 2001 SUPERSEDES: January 3, 2000 TELEPHONE NUMBER FOR INFORMATION (561) 585-2227 EMERGENCY TELEPHONE NUMBER Infotrac (800) 535-5053 Outside USA

Page 1 of 4

323-3500

TELEPHONE NUMBER FOR INFORMATION COUNTRY EMERGENCY TELEPHONE NUMBER

SECTION 2 - HAZARDOUS INGREDIENTS

HAZARDOUS COMPONENTS d-Limonene Orange oil terpenes Triethanolamine Silica, amorphous CAS # % (by weight) 1-5 OSHA PEL ppm I MUM' not established not established not established ACGIH TWA
ppm

MG/M'

SARA TITLE III

RQ LBS

5989-27-5 7 - 13 68647-72-3

102-71-60.5 - 1.5 7631-86-9 10 - 30

SECTION 3 - HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW
Cloudy liquid, lemon odor, contains abrasive materials. Will support combustion. Contact with eyes will cause irritation. Contact with skin may cause irritation. Hazard symbols for this product: Xi. Risk Phrases - R36 38

POTENTIAL HEALTH EFFECTS

INHALATION: High concentrations are irritating to the respiratory tract; may cause headache, dizziness, nausea, vomiting and malaise.

SKIN: Brief contact may cause slight irritation; prolonged contact may cause moderate irritation or dermatitis.

EYES: High vapor concentration or contact may cause irritation and discomfort.

INGESTION: May result in vomiting; aspiration of vomitus into the lungs must be avoided; DO NOT induce vomiting. Harmful or fatal if swallowed. CARCINOGENICITY ton
N o
WIG MONOGRAPHS?

No

OSHA REGULATED?

No

MATERIAL SAFETY DATA SHEET

PRODUCT NAME: MAVIDON LemonPrep rm
J

SECTION 4 - FIRST AID MEASURES

INHALATION: Remove affected person to fresh air; provide oxygen if breathing is difficult; if affected person is not breathing, administer CPR and seek emergency medical attention. SKIN: Remove contaminated clothing; wash affected area with soap and water; launder contaminated clothing before reuse; if irritation persists, seek medical attention. EYES: Remove contact lenses. Flush eyes with clear running water for 15 minutes while holding eyelids open; if irritation persists, seek medical attention. INGESTION: DO NOT induce vomiting; if vomiting occurs spontaneously, keep head below hips to prevent aspiration of liquid into lungs; seek immediate medical attention. Vomiting may be induced only under the supervision of a physician.

SECTION 5 - FIRE FIGHTING MEASURES

FLASH POINT (METHOD USED) > 200 F (> 93.3 C) FLAMMABLE LIMITS LELNot applicable UEL: Not applicable
/IIB

AUTOIGNITION TEMPERATURE: Not determined i NFPA CLASS: GENERAL HAZARDS: Product will support combustion. Products of combustion include compounds of carbon, hydrogen and oxygen, including carbon monoxide. EXTINGUISHING MEDIA Carbon dioxide, water fog, dry chemical, chemical foam FIRE FIGHTING PROCEDURES Self - contained respiratory equipment; cool containers to prevent pressure buildup and possible explosion when exposed to extreme heat. Caution - material will support combustion! UNUSUAL FIRE AND EXPLOSION HAZARDS Closed containers can explode due to buildup of pressure when exposed to extreme heat. HAZARDOUS COMBUSTION PRODUCTS Smoke, fumes, oxides of carbon

SECTION 6 - ENVIRONMENTAL RELEASE MEASURES

STEPS TO BE TAKEN IN CASE MATERIAL IS RELEASED OR SPILLED - CAUTION - WILL SUPPORT COMBUSTION. Do not wash to sanitary sewer. All spills - confine spill, soak up with approved absorbent shovel product into approved container for disposal. Flush area with water, recover flush for proper disposal.

SECTION 7 - HANDLING AND STORAGE

PRECAUTIONS TO BE TAKEN IN HANDLING AND STORAGE: Keep container closed when not in use; protect containers from abuse; protect from extreme temperatures, open flames. CAUTION - This material will support combustion. Keep this and other chemicals out of reach of children.

SECTION 8 - EXPOSURE CONTROLS I PERSONAL PROTECTION

ENGINEERING CONTROLS
The use of local exhaust ventilation is recommended to control emissions near the source. Provide mechanical ventilation of confined spaces. Use explosion-proof ventilation equipment. See Section 2 for Component Exposure Guidelines.

PERSONAL PROTECTION:
RESPIRATORY PROTECTION (SPECIFY TYPE): None required; however, if misting occurs, NIOSH approved respirator capable of removing particulate from air must be worn. Refer to 29 CFR 1910.134 or European Standard EN 149 for complete regulations. PROTECTIVE GLOVES: Neoprene or rubber gloves with cuffs. EYE PROTECTION: Safety goggles with side shields OTHER PROTECTIVE CLOTHING OR EQUIPMENT: Safety eyebath nearby WORK I HYGIENIC PRACTICES: Practice safe workplace habits. Minimize body contact with this, as well as all chemicals in general.

MATERIAL SAFETY DATA SHEET

PRODUCT October 29,NAME: 2001 MAVIDON LemonPrep P a g
TM

SECTION 15 - REGULATORY INFORMATION

TSCA (Toxic Substance Control Act) Components of this product are listed on the TSCA Inventory. SARA TITLE III (Superfund Amendments and Reauthorization Act) 311/312 Hazard Categories Acute health, possible eye irritant :313 Reportable Ingredients: None

CERCLA (Comprehensive Response Compensation and Liability Act) None

CPR (Canadian Controlled Products Regulations) This product has been classified in accordance with the hazard criteria of the Controlled Products Regulations and the MSDS contains all the information required by the Controlled Products Regulations IDL (Canadian Ingredient Disclosure List) Components of this product listed on the Canadian Ingredient Disclosure List are shown in Section 2. EINECS (European Inventory of Existing Commercial Chemical Substances) Components of this product are on the European Inventory of Existing Commercial Chemical Substances EC Risk Phrases R36 Irritating to eyes. R38 Irritating to skin. EC Safety Phrases 523 Do not breathe vapour. S24 Avoid contact with skin. S25 Avoid contact with eyes. S26 In case of contact with eyes, rinse immediately with plenty of water and seek medical advice. S28 After contact with skin, wash immediately with plenty of soap and water.

SECTION 16 - OTHER INFORMATION

No specific notes.

HMIS HAZARD RATINGS

HEALTH
FLAMMABILITY REACTIVITY

1
1

0
B

0 = INSIGNIFICANT 1 = SLIGHT 2 = MODERATE

Safety Glasses. Gloves

3 = HIGH 4 = EXTREME

P E R S O N A L P R O T E C T I V E E Q U IP M E N T

REVISION SUMMARY: This MSDS has been revised in the following sections: MSDS Prepared by:

Complete format revision

Comprehensive Data Base. Inc. P.O. Box 5604 Lakeland, FL 33807 USA (863) 644 - 3298 www.compdatabase.com

T h e i n fo r m a t i o n c o n t a i n e d h e r ei n i s b e l ie v e d to b e a c c u r a t e b u t i s no t w a r r a n t e d t o b e s o . Da t a a nd c a l c u la t i o n s a r e b a s e d o n info r mat i o n fur ni s he d b y t h e m a n u fa c tur e r o f t h e p r odu c t a n d m a n u fa ct u r e r s o f t h e c om p o ne n t s o f t h e p r o d u c t. U s e r s a r e a dv i s e d to co n fi r m i n ad v a n ce o f n e e d t h a t i n fo r m a t io n i s c u r r e n t , a pp li c a bl e a n d s u i t ed t o the c i r c u m s t a n c e s o f u s e . Ve n d or a s s u m e s n o r e s p o ns i b i l i t y f or i n jur y t o ve n d e e o r t h i r d p e r s o n s p r o xi m a t el y ca u s e d b y t h e m a t e ria l i f r e a s o n a bl e sa fe t y p r oc e d u re s a r e n o t a d h e r ed t o a s s t ip u l a t ed i n t h e d a t a s h e e t Fur t h e r m o r e , v en d o r a s s u m e s no responsibility for injury caused by abnormal use of this material even if reasonable safety procedures are followed. Any questions r egarding this product should be directed to the manufacturer of the product as described in Section 1.

MATERIAL SAFETY DATA SHEET

PRODUCT NAME: MAVIDON ACETONE
GENERAL USE: Solvent PRODUCT DESCRIPTION: Colorless liquid, extremely flammable

SECTION 1- PRODUCT AND COMPANY IDENTIFICATION

M a V
1

a on re

MANUFACTURER'S NAME Mavidon Medical Products ADDRESS (NUMBER. STREET, P.O. BOX) 2105 7th Avenue North (CITY, STATE AND ZIP CODE) Lake Worth, FL 33461DISTRIBUTOR'S NAME Same ADDRESS (NUMBER, STREET, P.O. BOX) (CITY, STATE AND ZIP CODE)

COUNTRY USA

DATE PREPARED: July 2, 2001 Page 1 of 4 SUPERSEDES: New TELEPHONE NUMBER FOR INFORMATION (561) 585-2227 EMERGENCY TELEPHONE NUMBER Infotrac 800 535-5053 Outside USA 352 323-3500

TEL E P H ON E N U MB ER F O R I N FOR M ATI O N COUNTRY USA EMERGENCY TELEPHONE NUMBER

SECTION 2 - HAZARDOUS INGREDIENTS

HAZARDOUS COMPONENTS
Acetone (a, b)

CAS #
67-64-1

OS H A P E L (by weight)
100

ACGIH TWA
P p m

SARA
TITLE III

RQ
LBS 5000

ppm
1000

1 MG/M3
2400

1 MG/M3

500

(a) See Section 15 (h) Indicates that the Resource Conservation and Recovery Act (RCRA) has determined the waste for this chemical is listed as hazardous and must be handled according to regulations in 40 CFR 260-281.

SECTION 3 - HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW
Colorless flammable liquid, potentially hazardous vapors. anesthetic effect leading to death in poorly ventilated areas Can cause eye and skin irritation upon contact. Inhalation of vapors can cause Hazard symbols for this product - F, XI, XN

POTENTIAL HEALTH EFFECTS

INHALATION: High concentrations are irritating to the respiratory tract, may cause headache, dizziness, nausea, vomiting and malaise.

SKIN: Brief contact may cause slight irritation; prolonged contact may cause moderate reddening, swelling and possible necrosis.

EYES: Contact causes severe irritation and pain associated with redness and swelling of the conjunctiva.

INGESTION: Moderately toxic; may cause headache, dizziness diarrhea and general weakness; large doses may result in red blood cell
hemolysis. CARCINOGENICITY
NIP?

No

!ARC MONOGRAPHS?

No

OSHA REGULATED?

No

MATERIAL SAFETY DATA SHEET

P P R O2. DU CT NAME: MAVIDON ACETONE July 2001 a g e 2 o f 4

SECTION 4 - FIRST AID MEASURES

INHALATION: Remove affected person to fresh air; provide oxygen if breathing is difficult; if affected person is not breathing, administer CPR and seek emergency medical attention. SKIN: Remove contaminated clothing; wash affected area with soap and water; launder contaminated clothing before reuse; if irritation persists, seek medical attention. EYES: Remove contact lenses. Flush eyes with clear running water for 15 minutes while holding eyelids open; if irritation persists, attention. INGESTION: Give two glasses of water for dilution; Induce vomiting by sticking fingers down throat; never give anything by mouth to an unconscious person; seek medical attention. seek medical

SECTION 5 - FIRE FIGHTING MEASURES

FLASH POINT (METHOD USED) -18 F (-27.8 C) TCC FLAMMABLE LIMITS LEL: 2.6% UEL: 12.8% IA AUTOIGNITION TEMPERATURE: Not determined I NFPA CLASS: GENERAL HAZARDS: Product is flammable. Products of combustion include compounds of carbon, hydrogen and oxygen, including carbon monoxide. EXTINGUISHING MEDIA Carbon dioxide, water fog, dry chemical, chemical foam FIRE FIGHTING PROCEDURES Firefighters must wear full facepiece self - contained breathing apparatus in positive pressure mode. Do not use solid stream of water since stream will scatter and spread fire. Fine water spray can be used to keep fire - exposed containers cool. UNUSUAL FIRE AND EXPLOSION HAZARDS Closed containers can explode due to buildup of pressure when exposed to extreme heat. Do not use direct stream of water on pool fires as product may reignite on water surface. Caution - Material is flammable! HAZARDOUS COMBUSTION PRODUCTS Smoke, fumes, oxides of carbon

SECTION 6 - ENVIRONMENTAL RELEASE MEASURES

STEPS TO BE TAKEN IN CASE MATERIAL IS RELEASED OR SPILLED . CAUTION - FLAMMABLE - Evacuate and ventilate area; confine and absorb into absorbent; place material into approved containers for disposal; for spills in excess of allowable limits notify the National Response Center (800) 424 - 8802; refer to CERCLA 40 CFR 302 for detailed instructions concerning reporting requirements.

SECTION 7 - HANDLING AND STORAGE

PRECAUTIONS TO BE TAKEN IN HANDLING AND STORAGE: Keep container closed when not in use; protect containers from abuse; protect from extreme temperatures. CAUTION - FLAMMABLE - keep away from all sources of ignition. "Empty" containers may contain residue which may form explosive vapors. Do not weld or cut near empty container that has not been professionally reconditioned. Use nonsparking tools when opening and closing containers. Maintain well ventilated work areas to minimize exposure when handling this material.

SECTION 8 - EXPOSURE CONTROLS I PERSONAL PROTECTION

ENGINEERING CONTROLS The use of local exhaust ventilation is recommended to control emissions near the source. Provide mechanical ventilation of confined spaces. Use explosion-proof ventilation equipment. See Section 2 for Component Exposure Guidelines. PERSONAL PROTECTION: RESPIRATORY PROTECTION (SPECIFY TYPE): None required while threshold limits (Section 2) are kept below maximum allowable concentrations: if TWA exceeds limits, NIOSH approved respirator must be worn. Refer to 29 CFR 1910.134 or European Standard EN 149 for complete regulations. PROTECTIVE GLOVES: Neoprene or rubber gloves with cuffs. EYE PROTECTION: Safety goggles with side shields OTHER PROTECTIVE CLOTHING OR EQUIPMENT: Safety eyebath nearby WORK / HYGIENIC PRACTICES: Practice safe workplace habits. Minimize body contact with this, as well as all chemicals in general.

MATERIAL SAFETY DATA SHEET

P R O D U CT NA ME : MAV I D ON A C E T O NE July 2, 2001 Page 3 of 4

SECTION 9 - PHYSICAL AND CHEMICAL PROPERTIES

VAPOR PRESSURE (MM Hg) 181 mm Hq A 20 C SPECIFIC GRAVITY (WATER = 1) 0/85 SOLUBILITY IN WATER Complete pH 7.0 BOILING POINT 133F (56.1 C) VISCOSITY Not listed
STABILITY INCOMPATIBILITY (MATERIALS TO AVOID): UNSTABLE: STABLE:

VAPOR DENSITY (AIR = 1) 2.0 EVAPORATION RATE (n-BUTYL ACETATE = 1) 7.7 FREEZING POINT Not determined APPEARANCE AND ODOR Clear water-white liquid, sweet pungent odor PHYSICAL STATE Liquid VOLATILE ORGANIC COMPOUNDS (Total VOC's) 6 5 pounds / gallon

SECTION 10 - STABILITY AND REACTIVITY

XXX CONDITIONS TO AVOID: Extreme temperatures, open flames, sparks

Strong oxidizers, strong acids HAZARDOUS DECOMPOSITION OR BYPRODUCTS: Decomposition will not occur if handled and stored properly In case of a fire, oxides of carbon, hydrocarbons, fumes, and smoke may be produced.
HAZARDOUS POLYMERIZATION MAY OCCUR: WILL NOT OCCUR: XXX CONDITIONS TO AVOID: None LD50 of Ingredient ( S p ec if y S pa d e s an d R ou t e) LC50 of I ngredient (Specify Species)

SECTION 11- TOXICOLOGICAL INFORMATION

Hazardous Ingredients Acetone (a,b) % 100 CAS # 67-64-1 9750 mg / kg Oral - rat 16,000 ppm / 4 hr Inhalation - rat

SECTION 12 - ECOLOGICAL INFORMATION

No data are available on the adverse effects of this material on the environment. Neither COD nor BOD data are available. Based on the chemical composition of this product it is assumed that the mixture can be treated in an acclimatized biological waste treatment plant system in limited quantities. However, such treatment should be evaluated and approved for each specific biological system. None of the ingredients in this mixture are classified as a Marine Pollutant.

SECTION 13 - DISPOSAL CONSIDERATIONS

WASTE DISPOSAL METHOD: Dispose of in accordance with Local, State, and Federal Regulations. This product may produce concentrated hazardous vapors or fumes in a disposal container creating a dangerous environment. Refer to "40 CFR Protection of Environment Parts 260 299" for complete waste disposal regulations for ignitable materials. Consult your local, state, or Federal Environmental Protection Agency before disposing of any chemicals. Do not flush to sanitary sewer or waterway.

SECTION 14 - TRANSPORT INFORMATION

PROPER SHIPPING NAME: Acetone

HAZARD CLASS / Pack Group: 3 / II REFERENCE: 49 CFR 173.150..202, .242 IDENTIFICATION NUMBER: UN 1090 LABEL: FLAMMABLE LIQUID

IATA HAZARD CLASS / Pack Group: 3 / II IMDG HAZARD CLASS: 3 / II RID/ADR Dangerous Goods Code: 3 Canadian TDG Class / Division: 3.2

HAZARD SYMBOLS: F Note: Transportation information provided is for reference only. Client is urged to consult CFR 49 parts 100 - 177, IMDG. IATA, EC, Canadian TDG. and United Nations TDG information manuals for detailed regulations and exceptions covering specific container sizes, packaging materials and methods of shipping.

MATERIAL SAFETY DATA SHEET

PRODUCT NAME: MAVIDON ACETONE July 2, 2001 Page 4 of 4

SECTION 15 - REGULATORY INFORMATION

TSCA (Toxic substance Control Act) Components of this product are listed on the TSCA Inventory. SARA TITLE Ill (Superfund Amendments and Reauthorization Act) 311/312 Hazard Categories Acute health, flammable 313 Reportable Ingredients: None

CERCLA (Comprehensive Response Compensation and Liability Act) (b) The Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) has notification requirements for releases or spills to the environment of the Reportable Quantity (RQ for this mixture = 5000 Ibs) or greater amounts, according to 40 CFR 302. CPR (Canadian Controlled Products Regulations This product has been classified in accordance with the hazard criteria of the Controlled Products Regulations and the MSDS contains all the information required by the Controlled Products Regulations IDL (Canadian Ingredient Disclosure List Components of this product listed on the Canadian Ingredient Disclosure List are shown in Section 2. EINECS (European Inventory of Existing Commercial Chemical Substances Components of this product are on the European Inventory of Existing Commercial Chemical Substances EC Risk Phrases R11 Highly flammable R20 Harmful by inhalation R36 Irritating to eyes R38 Irritating to skin. EC Safety Phrases S16 Keep away from sources of ignition S23 Do not breathe vapor S25 Avoid contact with eyes S28 After contact with skin, wash immediately with plenty of soap al 529 Do not empty into drains

SECTION 16 - OTHER INFORMATION

No specific notes.

HMIS HAZARD RATINGS

HEALTH FLAMMABILITY REACTIVITY

1 3 0 B

0 = INSIGNIFICANT 1 = SLIGHT 2 = MODERATE Safety Glasses. Gloves

3 = HIGH
4 = E X T R E ME

P E R S O N A L P R O T E C T I V E E Q U IP M E N T

REVISION SUMMARY:

This MSDS has been revised in the following sections: No revisions available

MSDS Prepared by:

Comprehensive Data Base, Inc. P.O. Box 5604 Lakeland, FL 33807 USA (863) 644 - 3298 www.compdatabase.com

T h e i n fo r m a t i o n c o n t a i n e d h e r e i n i s b e l i e v e d t o be a c c u r a t e b u t i s n o t w a r r a n t e d t o b e s o . U s e r s a r e a d v i s e d t o c on fi r m i n a d v a n c e o f n e e d t h a i n fo r m a t io n i s c u r r e n t , ap p li c a bl e a n d s u i t ed t o the c i r c u m s t a n c e s o f u s e . Ve n do r a s s u m e s n o r e s p o ns i b i l i t y fo r i n jur y t o ve n d e e o r t h i r d p e r s o n s p r o xi m a t el y ca u s e d b y t h e ma t e r ia l i f r ea s o n a bl e sa fe t y p r o ce du r e s a r e n o t ad h e r e d to a s s t i p u la t e d In t h e d a t a s h e e t . Fur t h e r mo r e , v end o r a ssum e s no responsibility for injury caused by abnormal use of this material even if reasonable safety procedure s are followed.

MATERIAL SAFETY DATA SHEET

PRODUCT NAME: Collodion Remover
GENERAL USE: Collodion Remover PRODUCT DESCRIPTION: Colorless liquid, combustible, sweet ether odor

SECTION 1 - PRODUCT AND COMPANY IDENTIFICATION

MANUFACTURER'S NAME Mavidon Medical Products ADDRESS (NUMBER, STREET, P.O. BOX) 2105 7th Avenue North (CITY, STATE AND ZIP CODE) Lake Worth, FL 33461DISTRIBUTOR'S NAME Same ADDRESS (NUMBER, STREET, P.O. BOX) (CITY, STATE AND ZIP CODE)

COUNTRY USA

DATE PREPARED: February 25, 2001 Page 1 of 4 SUPERSEDES: New TELEPHONE NUMBER FOR INFORMATION (561) 585-2227 EMERGENCY TELEPHONE NUMBER Infotrac (800) 535-5053 Outside USA (352) 323-3500

TELEPHONE NUMBER FOR INFORMATION COUNTRY EMERGENCY TELEPHONE NUMBER

SECTION 2 - HAZARDOUS INGREDIENTS

HAZARDOUS COMPONENTS Proprietary Ingredient (a) Ethanol CAS # Not specified 64-17-5 %
(by weight)

OSHA PEL
ppm I MG/M"

ACGIH TWA
ppm MG/M3

SARA
TITLE III

RQ LBS

75 - 95 1-5 1000

not established 1900 1000

No

(a) The specific product is not identified due to "Trade Secret" status. In emergency situations further information may be obtained by the on - duly physician calling the emergency information number listed above. Reference 29 CFR 1910.1200 and / or 40 CFR 350.

SECTION 3 - HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW
Colorless liquid, combustible, low order of toxicity, may cause slight irritation upon contact with eyes or skin. Exposure to vapors not a likely hazard.

POTENTIAL HEALTH EFFECTS

INHALATION: Exposure to vapors not likely. High concentrations may be irritating to the respiratory tract; may cause headache, dizziness nausea, vomiting and malaise. SKIN: Brief contact may cause slight irritation; prolonged contact may cause moderate irritation.

EYES: Contact may cause slight temporary irritation. Corneal injury is unlikely.

INGESTION: Small amounts ingested are not likely to cause injury. Ingestion of large amounts may cause headache, dizziness diarrhea and general weakness.
CARCINOGENICITY NM" NO IARC MONOGRAPHS? No OSHA REGULATED? No

MATERIAL SAFETY DAT A SHEET

PRODUCT NAME: Collodion Remover February 25, 2001 Page 2 of 4

SECTION 4 - FIRST AID MEASURES

INHALATION: Remove affected person to fresh air; provide and seek emergency medical attention. SKIN: Remove contaminated clothing; wash affected area with soap and water; launder contaminated clothing before reuse; if irritation persists, seek medical attention. EYES: Remove contact lenses. Flush eyes with clear running water for 15 minutes while holding eyelids open, if irritation persists, seek medical attention. INGESTION: Do not induce vomiting unless directed to do so by medical personnel; never give anything by mouth to an unconscious person; seek medical attention. oxygen if breathing is difficult; if affected person is not breathing, administer CPR

SECTION 5 - FIRE FIGHTING MEASURES

FLASH POINT (METHOD USED) 176 F (80 C) TCC FLAMMABLE LIMITS LEL; 1 2% UEL: 5.4% AUTOIGNITION TEMPERATURE: Not determined 1 NFPA CLASS: IIA GENERAL HAZARDS: Product is combustible. Products of combustion include compounds of carbon, hydrogen and oxygen, including carbon monoxide. EXTINGUISHING MEDIA Carbon dioxide, water, water fog, dry chemical, chemical foam FIRE FIGHTING PROCEDURES Self - contained respiratory equipment; cool containers to prevent pressure buildup and possible explosion when exposed to extreme heat. Caution - material is combustible! UNUSUAL FIRE AND EXPLOSION HAZARDS Closed containers can explode due to buildup of pressure when exposed to extreme heat. HAZARDOUS COMBUSTION PRODUCTS Smoke, fumes, oxides of carbon

SECTION 6 - ENVIRONMENTAL RELEASE MEASURES

STEPS TO BE TAKEN IN CASE MATERIAL IS RELEASED OR SPILLED; COMBUSTIBLE - Evacuate and ventilate area; remove all sources of sparks, ignition and open flames: confine and absorb into approved absorbent; place material into approved containers for disposal; do not wash to sewer or waterway.

SECTION 7 - HANDLING AND STORAGE

PRECAUTIONS TO BE TAKEN IN HANDLING AND STORAGE: This material is combustible. It should be stored in tightly closed containers in a cool, well ventilated area. Vapor may form explosive mixtures in air. All sources of ignition should be controlled. Keep this and other chemicals out of reach of children. Avoid inhaling concentrated fumes or vapors.

SECTION 8 - EXPOSURE CONTROLS I PERSONAL PROTECTION

ENGINEERING CONTROLS The use of local exhaust ventilation is recommended to control emissions near the source. Provide mechanical ventilation of confined spaces. Use explosion-proof ventilation equipment. See Section 2 for Component Exposure Guidelines. PERSONAL PROTECTION: RESPIRATORY PROTECTION (SPECIFY TYPE): None required while threshold limits (Section 2) are kept below maximum allowable concentrations; if TWA exceeds limits, NIOSH approved respirator must be worn. Refer to 29 CFR 1910.134 or European Standard EN 149 for complete regulations. PROTECTIVE GLOVES: Neoprene or rubber gloves with cuffs. EYE PROTECTION: Goggles with side shields; safety eyebath nearby. OTHER PROTECTIVE CLOTHING OR EQUIPMENT: Coveralls, apron, or other equipment should be worn to minimize skin contact. WORK / HYGIENIC PRACTICES: Practice safe workplace habits. Minimize body contact with this, as well as all chemicals in general.

MATERIAL SAFETY DATA SHEET

PRODUCT NAME: Collodion Remover February 25, 2001 Page 3 of 4

SECTION 9 - PHYSICAL AND CHEMICAL PROPERTIES

VAPOR PRESSURE (MM Hg) < 0.1 mm Hg krfi 20 C SPECIFIC GRAVITY (WATER = 1) 0.972 SOLUBILITY IN WATER Appreciable (> 20%) pH Not applicable BOILING POINT 408F (209" C) VISCOSITY Approximately that of water
STABILITY INCOMPATIBILITY (MATERIALS TO AVOID): UNSTABLE: STABLE XXX

VAPOR DENSITY (AIR = 1) 6.6 EVAPORATION RATE (WATER = 1) <1 FREEZING POINT Not determined APPEARANCE AND ODOR Colorless liquid, sweet ether odor PHYSICAL STATE Liquid VOLATILE ORGANIC COMPOUNDS (Total VOC's) 8.12 lbs / gallon
CONDITIONS TO AVOID: Extreme temperatures, open flames

SECTION 10 - STABILITY AND REACTIVITY

Strong oxidizers, strong acids HAZARDOUS DECOMPOSITION OR BYPRODUCTS: Decomposition will not occur if handled and stored properly. In case of a fire, oxides of carbon, hydrocarbons, fumes, and smoke may be produced.
HAZARDOUS P OLYMERIZAT ION MAY OCCUR: WILL NOT OCCUR: XXX CONDITIONS TO AVOID: None

SECTION 11- TOXICOLOGICAL INFORMATION

Hazardous Ingredients Proprietary Ingredient (a) Ethanol % 75 - 95
1-5

CAS # Not specified 64-17-5

LD50 of Ingredient (Specify Species and Route)

LC50 of Ingredient (Specify Species)

> 5000 mg / kg Oral - rat 3450 mg / kg Oral - mouse

Not established 20,000 ppm / 1014 Inhalation - rat

SECTION 12 - ECOLOGICAL INFORMATION

No data are available on the adverse effects of this material on the environment. Neither COD nor BOD data are available. Based on the chemical composition of this product it is assumed that the mixture can be treated in an acclimatized biological waste treatment plant system in limited quantities. However, such treatment should be evaluated and approved for each specific biological system. None of the ingredients in this mixture are classified as a Marine Pollutant.

SECTION 13 - DISPOSAL CONSIDERATIONS

WASTE DISPOSAL METHOD: Dispose of in accordance with Local, State, and Federal Regulations. This product may produce concentrated hazardous vapors or fumes in a disposal container creating a dangerous environment. Refer to "40 CFR Protection of Environment Parts 260 299" for complete waste disposal regulations for ignitable materials. Consult your local, state, or Federal Environmental Protection Agency before disposing of any chemicals. Do not flush to sanitary sewer or waterway.

SECTION 14 - TRANSPORT INFORMATION

PROPER SHIPPING NAME: Not Regulated

HAZARD CLASS / Pack Group: None / None

IATA HAZARD CLASS / Pack Group: None IMDG HAZARD CLASS: None IDENTIFICATION NUMBER: None RID/ADR Dangerous Goods Code: None LABEL: None Required Canadian TDG Class / Division: None HAZARD SYMBOLS: None Note: Transportation information provided is for reference only. Client is urged to consult CFR 49 parts 100 - 177, IMDG, IATA, EC, Canadian TDG, and United Nations TDG information manuals for detailed regulations and exceptions covering specific container sizes, packaging materials and methods of shipping. REFERENCE: Not Applicable

MATERIAL SAFETY DATA SHEET

PRODUCT NAME: Collodion Remover February 25, 2001 Page 4 of 4

SECTION 15 - REGULATORY INFORMATION

TSCA (Toxic substance Control Act) Components of this product are listed on the TSCA Inventory. SARA TITLE III (Superfund Amendments and Reauthorization Act) 311/312 Hazard Categories None 313 Reportable Ingredients: None

CERCLA (Comprehensive Response Compensation and Liability Act) None

CPR (Canadian Controlled Products Regulations This product has been classified in accordance with the hazard criteria of the Controlled Products Regulations and the MSDS contains all the information required by the Controlled Products Regulations IDL (Canadian Ingredient Disclosure List Components of this product listed on the Canadian Ingredient Disclosure List are shown in Section 2. EINECS (European Inventory of Existing Commercial Chemical Substances Components of this product are on the European Inventory of Existing Commercial Chemical Substances EC Risk Phrases EC Safety Phrases S16 Keep away from sources of ignition.

SECTION 16 - OTHER INFORMATION

No specific notes.

HMIS HAZARD RATINGS

HEALTH FLAMMABILITY REACTIVITY

0 2 0 C

0 = INSIGNIFICANT

3 = HIGH
4 = EXTREME

1 = SLIGHT
2 = MODERATE Safety Glasses. Gloves. Apron

PERSONAL PROTECTIVE EQUIPMENT REV ISI ON SU MM AR Y:

This MSDS has been revised in the following sections: No revisions available

MSDS Prepared by:

Comprehensive Data Base, Inc. P.O. Box 5604 Lakeland, F L 33807 USA (863) 644 - 3298 www.compdatabase.com

The information contained herein is believed to be accurate but is not warranted to be so. Users are advised to confirm in advance of need tha
information is current, applicable and suited to the circumstances of use. Vendor assumes no responsibility for injury to vendee or third persons proximately caused by the material if reasonable safety procedures are not adhered to as stipulated In the data sheet. Furthermore, vendor assumes no responsibility for injury caused by abnormal use of this material even if reasonable safety procedures are followed.

Stanford Hospital and Clinics NeuroDiagnostic Laboratories

Policies and Procedures (Rev. 02/2009)

Administration The administrative leadership of the NDL consists of the following: Clinical Director Manager Medical Director Divisions The divisions of the NDL and their respective heads are as follows: Electroencephalography (EEG) Electromyography (EMG(NCV) Evoked Potentials (EP) Intraoperative Monitoring (IOM) Transcranial Ultrasound (TCD) Neuropsychology (Npsy) Hours of Operation The Stanford NeuroDiagnostic Laboratories (NDL) are open from 8:00 am until 5:00 pm Monday through Friday, except holidays. Urgent or emergent procedures may be performed outside normal hours of operation. Robert Fisher, MD, PhD Les Dorfman, MD Les Dorfman, MD Jaime Lopez, MD Maarten Lansberg, MD Penelope Zeifert, PhD Alison Kerr, RN Mark Burdelle, REEGT Les Dorfman, MD

Referral

Patients are ordinarily scheduled for testing on referral from a treating physician on the SW medical staff.
Exceptions to the referral policy may be made at the discretion of the relevant division head.

Registration Patients for examination in the NDL must be concurrently registered in SHC. Authorization Insurance authorization for NDL procedures must be obtained by the referring healthcare provider.

Charges Charges for the various services rendered in the NDL are listed in the SHC directory of Charges. Health and Safety The staff of the NDL adhere to the procedures set forth in the SHC Health and Safety Manuals. Controlled Substances Controlled substances in the NDL are handled according to the procedures recommended in the SHC Pharmacy Manual.

Reports Reports of test results are generated timely and sent to the patient's medical record and/or referring physician(s). Records Copies of test reports are retained in the NDL as required by SHC policy and state law.

DEPARTMENT OF NEUROLOGY AND NEUROLOGICAL SCIENCES

STANFORD UNIVERSITY MEDICAL CENTER

S t a n fo r d U n i v e r si t y H o s p i t al a n d C l i n i c s Lucille Salter Packard Children's Hospital 300 Pasteur Drive, Rm. A343 Stanford, CA 94305-5235

BOTULINUM TOXIN POLICY AND PROCEDURES NEURODIAGNOSTIC LABS

Patients receiving Botulinum injections in the Neurodiagnostic Labs are seen for initial evaluation by the performing neurologist prior to first injection. A history is obtained and examination performed. The patient is advised of the benefits, risks and side effects of the medication prior to first injections. Botulinum injections performed in the Neurodiagnostic Labs are performed for medically indicated conditions only, including but not limited to torticollis, dystonia, blepharospasm, hemifaciai spasm, and spasticity. Injections are performed in the Neurodiagnostic Labs. Medication is stored in a refrigerator/freezer located in Room H-3136 and kept in accordance with manufacture's specifications. A daily temperature log is maintained. Any outdated medication is returned to the pharmacy for disposal. The injections are performed using sterile technique and mixed according to the manufacture's specifications. Medication that is not used is destroyed under Stanford Hospital and manufacturer's guidelines. When medically indicated Botulinum toxin injections are performed under EMG guidance. Following injections the patient remains in the Neurodiagnostic Lab for 15-30 minutes to monitor for any side effects from the medication. Patients are advised to contact the treating physician should there be any side effects noted.

Re-treatment is performed when patients note return of symptoms, however, not prior to three months from previous treatment according to the manufacture's guidelines. Records are maintained in the Neurodiagnostie Lab including a i1otuhututu Toxin world/test indicating muscles injected and amounts given A separate log is maintained for any studies being performed using flotulinunt Toxin A and B. Informed consent is obtained and copies are kept by the study coordinator. Separate temperature lop are maintained as well as patient and injection site information. Further information may be obtained by contacting the Neurodiagnostic Labs at 7234$1111.
Upland 012002

I Stanford University Medical Center Department of Neurology

Bonilinion Toxin Therapy Progress Record

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STANFORD UNIVERSITY HOSPITAL WADA/EEG WORKSHEET EEG#: NAME: MR#: HANDEDNESS: HISTORY: DATE: TIME: DOB: PHYSICIAN: CURRENT MEDICATIONS: TECH: AGE/SEX:

MEDS FOR WADA: INJECTION TIME L HEMISPHERE:

GLOSSARY OF TERMS

INJECTION TIME R HEMISPHERE:

Artillery = A Snowman = Please Sit Down = PSD No Ifs Ands Or Buts = NIAOB

SM Gingerbread = GB

The Sun Rises In The East = TSRITE

CLINICAL NOTES:

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Lucile Packard Children's Hospital at Stanford

Child's Name:

Department of Neurology Video EEG Seizure Log

Date Time 5/21 Brief Description of Seizure Example: "Body stiffened and shook" 0:20 AM Mom Name

10:15 PM

Example: "Stared. Didn't respond when I called his name." J. Doe, RN

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EMU SAFETY AID TRAINING Stanford Medical Center

Goal: To provide didactic information about: 1. Fundamentals of patient care; 2. Epilepsy and seizures; 3. EEG, in order to facilitate the job of caring for Stanford inpatients with seizures. EMU Safety Aid Training Schedule Week 1 Orientation Basic Patient Care Procedures Week 2 Day 1: Out of the Shadows video 1 hour Discussion and quiz 1 hour 4 minute video series 01. Understanding epilepsy 02. Types of seizures 03. Understanding partial seizures 04. Understanding generalized seizures 05. What causes epilepsy 06. How is epilepsy diagnosed? 07. Ten truths about epilepsy 08. Epilepsy through the ages 09. Genetic causes of epilepsy 10. Febrile seizures 11. Seizures from strokes 12. Seizures from head trauma 13. Seizure imitators overview 14. Consciousness imitators of seizures 15. Confusion imitators of seizures 16. Movement imitators of seizures

Alison Kerr Alison Kerr

Robert Fisher Robert Fisher Robert Fisher

Day 2: Part 2 videos Robert Fisher 17. Psychological imitators of seizures 18. Understanding psychogenic non-epileptic seizures 19. Treating psychogenic nonepileptic seizures 20. Approaches to seizure medication 21. Who gets epilepsy surgery? 22. Your pre-surgical assessment, part 1 23. Your pre-surgical assessment, part 2 24. Resective surgery for the treatment of epilepsy 25. Other types of epilepsy surgery 26. Risks and benefits of surgery, part 1 27. Risks and benefits of surgery, part 2 157

28. 29. 30. 31.

Safe driving for people with epilepsy Epilepsy and employment Epilepsy and safety Recreation safety for people with epilepsy Robert Fisher Harinder Kaur Mimi Callanan Mimi Callanan Harinder Kaur Harinder Kaur Harinder Kaur Harinder Kaur

Day 3: Introduction to EEG The EEG machine and patient hook-up Day 4: Recognizing Seizures EMU Procedures Day 5: Tech Tag-along Day 6: Tech Tag-along Day 7: Tech Tag-along Day 8: Tech Tag-along

Section 1: Basic patient care procedures To be added

Section 2: Seizures and epilepsy

A. Review the Out of the Shadows lecture by Dr. Fisher 1 hour., see printed transcript
Questions and answers, discussion 30 minutes.

OUT OF THE SHADOWS VIDEO LECTURE TRANSCRIPT Dr. Robert S. Fisher Stanford
We are going to talk today about epilepsy, which is one of the most misunderstood conditions in medical science. Its official definition is that of recurrent, spontaneous seizures. A seizure is a transient disorder, signs and symptoms, due to abnormal or excessive synchronous electrical activity of the brain - in other words, an electrical storm in the brain. The word "seized" has been connoted over the centuries to be seized by supernatural forces, either the Gods or the Devil. The word

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"seized" in Greek means to be taken hold. When they came to the crowd a man approached Jesus and knelt before him. Lord have Mercy on my son, he said. He has seizures and is suffering greatly. Jesus rebuked the demon, and it came out of the boy, and he was healed from that moment. Of course, epilepsy is nothing more and nothing less than a medical disorder, just like multiple sclerosis, or muscular dystrophy, and yet it carries all the stigma, all this baggage. What epilepsy is not: it's not mental retardation, its not alcoholism, psychosis, violence, criminal behavior or contagious. It is, however, common. It is in fact the most prevalent serious neurological illness able to affect people of all ages, from the young to the old. The condition of status epilepticus, which is not ordinary seizures, but seizures that go on for more than half an hour without stopping, claim from 10,000 to 30,000 lives per year, either from the seizures or the underlying condition causing the seizures. Epilepsy has onset peaks in the young and the old. Should you be fortunate enough to live to age 75, which I hope you will be, you will have a 10% chance of having a least one seizure in your life. This is a common condition, but because of the stigma, people do not wear it on their sleeve for everyone to notice. Many famous people are said to have epilepsy; of course, how can we really know about some of these? Its an interesting list, with a story behind each one. About 1% of the world's population has epilepsy. It occurs in US Supreme Court justices, and perhaps of more interest to those of us here at Stanford, it occurs in Stanford quarterbacks. He just had a seizure a few days ago, the first one, and therefore he will be missing the Saturday game with USC, which I am sure we would have won (note added: actually we did win with the backup quarterback, a great upset!). Epilepsy is far from being a solved problem. Those people with seizures who respond to old-time existing medications are about one out of two. Then, those who respond to new medications, and new ones come out all the time, are about 10%. About 5% of people are candidates for brain surgery to attempt to cure the epilepsy. This involves removal of the seizure focus, the part of the brain from which seizures come. I'll say more about that later. About a third remains uncontrolled, no matter what we do. The hope for this uncontrolled group, is research: inventing new and better methods to treat seizures. We are trying all the time. Considering the one-third of people who are not controlled, it is a very large number, because of the high prevalence of epilepsy. It is a greater number than people with all brain tumors primary or metastatic, plus all multiple sclerosis, plus muscular dystrophy, plus all GuillainBarr, plus all Lou Gehrig's disease, put together. It is a group in substantial need. Life is no fun with uncontrolled seizures or with substantial toxicity from seizure medications. Those who are not controlled or who are not feeling well on their medications, those who have a poor quality of life because of seizures, should be

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evaluated at a Comprehensive Epilepsy Center, where there can be outpatient clinical evaluations, various tests, hospital admissions to control the seizures, video-EEG monitoring, and sometimes (in about 5%) epilepsy surgery. There should be psychological support and neuropsychological testing, education and research. Most big cities do have one or two Comprehensive Epilepsy Centers. Stanford has certainly been one for a long time. Now we go into what I teach my medical students and residents. When I see a patient who might have epilepsy in clinic or in the hospital, I go through a series of logical steps. The first one is to consider whether the person is in fact having a seizure, because everything that goes bump in the night is not necessarily a seizure. We will do these points one-by-one. There many imitators of epilepsy, some of them are medical, some of them are neurological and some are psychological. Fainting spells, which are medically called syncope, can drop a person to the ground and look like seizures, as can heart irregularities, low blood sugar, and low oxygen. Ministrokes can look like seizures. Migraine is not just a headache but may cause confusion episodes. Sleep disorders such as narcolepsy, people who fall asleep inappropriately, may be thought to have seizures. Dizziness, movement disorders, tremor, tics, dystonia, abnormal posturing, have been confused with seizures. And then a variety of psychological events can look like seizures, including those called pseudo-seizures or nonepileptic seizures, which are in my view a type of cry for help. People with nonepileptic seizures are not faking a seizure, rather they are involuntarily responding to accumulated stress by producing something that looks very much like a seizure. People have been referred to me for epilepsy surgery after years of uncontrolled epilepsy, who have never had epilepsy at all, but had had one of the imitators. In medicine its always good to start with a proper diagnosis. The diagnosis in epilepsy is not high tech. Diagnosis starts with a good story of something that sounds like seizures: an alteration of sensory or motor function, behavior or consciousness, punched out in time, with a clear start and a clear finish, and a time course lasting five seconds to five minutes. A seizure is reasonably stereotyped, meaning the same event-to-event. It is rarely triggered. If Johnny has a seizure every time his brother, Jimmy, grabs his toy, it is not epilepsy, it is a behavioral event. However, occasional seizures can be triggered by the environment, for example flashing lights. A seizure should be distinguished from the imitators of epilepsy that I just mentioned. The physical exam, which is so important in medicine and neurology, is relatively less so in the diagnosis of epilepsy, because epilepsy diagnosis is so much about the story. I tell my medical students that the most important tool that they have to examine people with epilepsy is the telephone, so they can call someone who has actually seen the episode and get a good description. Occasionally, something shows up on the physical examination that points to a part of the brain that may have been injured, a toxicity of medication, or a clue to some genetic or hereditary disease that might be causing the seizures.

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Among tests, the most important test is the EEG - electroencephalogram, brainwaves. When we do an EEG on someone, we look for spikes. The electrodes are placed on the head according to standard nomenclature, with odds on the left and evens on the right. Here we see spikes mainly on the right side of the brain. This whole frame is 10 seconds in time, and so spikes are so brief that the person would not feel them. They reflect synchronous abnormal firing of neurons for a fraction of a second, and they mark the part of the brain that might give rise to seizures. If the spikes or abnormal brain rhythms persisted for longer period of time, such as we see elow, going on for about 5 seconds, then the person would have symptoms and they would start to have what visibly would be a seizure. The nature of the seizure would depend upon where in the brain the abnormal electricity was. If it occurred in a motor area controlling the right arm, there might be twitching of the right arm. If it occurred in visual cortex, there would be visions. If it occurred in temporal lobe parts of the brain that have to do with memory, there would be confusion or sometimes strange, forced abnormal memories. Deep temporal lobe structures also are linked to emotionality. You can imagine, when someone has unexplained spontaneous emotional sensations or forced memories, during the years when epilepsy was not understood, such people got locked up in a mental institution for their seizures. It still happens, but thankfully not as much. We can study the seizures in an epilepsy monitoring unit, recording video, sound and EEG, in order to correlate the behavioral event with the brainwave activity. It sometimes helps us to make a diagnosis, where one was just not clear from the description. The next question is, if a seizure, what type? There is a complex tree of the types of seizures. The main branches are for those that start partially, which is a synonym for focally, and those that seem to start all over at once, called generalized. If we are looking at the brainwave pattern during a generalized seizure, it lights up like a Christmas tree, right and left, front and back. Typically, there would be unconsciousness from the beginning. With partial seizures, sometimes there is a warning - which is called an aura, but in generalized seizures awareness typically is out like turning off a light.

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If you look at the next level of branches, partial seizures are either simple or complex. Complex does not mean complicated. It means there is loss of consciousness, awareness or memory. If a person becomes confused with the partial seizure, then it is a complex partial seizure. If a person says Doc, my hands twitching, it's been doing this for a couple of hours - it's annoying, can you get it stopped, then it is a simple partial seizure: there is no alteration of consciousness or awareness. Any seizure that start partially can spread throughout the entire brain, and then it becomes secondarily generalized. You may have a seizure deep in the temporal lobe, one of the four lobes of the brain and the most seizure-prone part of the brain. When the seizure stays localized to the left or right temporal lobe, a person might just feel funny feelings, dj vu ( Ive been here before), odd memories, emotionality, or gastrointestinal sensations, such as nausea. These are focal seizure sensations from the temporal lobe. When the abnormal electrical activity spreads to both temporal lobes, then there is impaired ability to register memory producing a dream-like state, and sometimes a robot-like performance, living in an odd world that must be second-to-second in duration. If the activity spreads to the entire brain including motor centers, then there is a full generalized seizure with shaking. This type of seizure used to be called grand mal, but it is officially called tonicclonic, with tonic meaning stiffening and clonic meaning jerking. In a few moments I will show you some of those to make them clearer. There are other generalized seizure types besides tonic-clonic. A petit mal seizure, which is now called an absence seizure is a brief staring spell with interruption of activity. The synchronous spike and wave activity on the EEG involves much of the brain. A myoclonic seizure is a sudden jerk or twitch. Myoclonic means muscle jerk. It is a very brief seizure, but one that is still generalized. An atonic seizure is a loss of muscle tone, resulting in a sudden drop, what one of my Baltimore patients back in my Johns Hopkins days once called the atomic seizures. You can fall pretty hard with an atonic seizure. Let me now show you some of these seizures. I emphasize two things: one is that all of these are with permission to be shown in public; and the second is that the seizures can be upsetting to watch. But I think it is important to see the nature of the beast - what we are fighting. First is a simple partial seizure (see accompanying video on www.epilepsy.com ). There is a lot of shaking, but he is with it enough to hit the button to call the nurse and alert her of a seizure. He can respond and answer, he's fully with it. Therefore, this is a simple partial seizure. He had surgery on the small area of the brain that was generating the seizures and the seizures are now gone. The next event is a complex partial seizure. Notice the rhythmical pulling-fumbling hand motions. That's called an automatism, an automatic activity. This woman worked in a care home for the elderly, and while she was putting an around the neck of an elderly woman, she had a seizure. She was struggling and pulling on the apron and those in the nursing home thought she was somehow attacking this woman. So they shouted to her, but did not hear-she was in the middle of a complex partial seizure, and she was confused. Observers tackled her and she subsequently

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was charged with elder abuse. In some miscarriage of justice which happened before I met her, the judge would not allow evidence in court about her epilepsy, and she ended up serving time in jail. Here you have another example of how misunderstood epilepsy can be. This next seizure is upsetting to watch. It is a tonic-clonic seizure, the most vigorous form of a seizure. Next, this teenager is playing a video game and in comes a brain discharge. He stopped pushing the game buttons, and his head is nodding a little bit. You can see that high-voltage storm of spikes and waves all over the head in the EEG. That was a petit mal seizure, also called an absence seizure. This woman just fell forward from an atonic seizure: she would have been on the ground had she been standing. Those are the main seizure types. There are others and there are many variants. In fact, no two people have exactly the same type of seizure, because no two people have exactly the same type of brain. Seeing some of these can give you some idea of how upsetting seizures can be. It has been my experience, vicariously, because I have never personally had a seizure, that family members often find the seizures more difficult than does the person having them. Some in this room may know this much better than do I. The person having the seizure sometimes is out of it and doesn't know of the seizure except for confusion, soreness and embarrassment afterwards. The first time a family member sees a child, husband, wife, parent having a seizure, it's hard to believe that they are not dying. But they are not. A seizure rarely harms the brain and rarely causes death. I can't say never. You can crash a car or fall down a flight of stairs or have a heart attack during a seizure. A seizure actually is less damaging to the brain than is a stroke, where brain cells do die. We classify seizures, because classification tells us how best to treat and how to do enact the medical the work-up. We rule out serious causes. Only about half of the time can we find the cause of the seizure. As our neuroimaging is getting better, it might be 60% now, and soon it will be 9095%, but some of the injuries that cause seizures are microscopic and we can not see them on MRIs or CT scans. That virus that got in when you had a headache and bad flu and couldn't think, that left a scar. The head trauma that you didn't think was significant but it might be. Or a genetic condition that has changed the chemistry of the brain, which we have no way yet to image, is causing an imbalance between brain excitation and inhibition, leading to a seizure. The MRI is a brain imaging technique that can reveal a structural problem that might be causing seizures. Sometimes, the problem is too small to be seen. Or seizures could come from a genetic or chemical cause, which will not show on the MRI. Seizures

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can be caused either by nature or nurture. The causes for seizures are different in different ages. Idiopathic means cause unknown This MRI shows a common cause in society, which is head trauma causing seizures. There is scarring in the frontal lobes where there was a coup or contra-coup injury with the frontal lobes bumping against the inside of the skull with the trauma. This is the signature injury of the Iraq war, and there will be more and more people who will be having seizures coming back from Iraq with head trauma. The next MRI shows an old stroke. Strokes can cause seizures. Next is an MRI with a blood clot, a hematoma pressing on the brain, which can cause seizures. Next is an abnormal blood vessel called a hemangioma, little raspberry-like varicose vessel of the brain. Here's a brain abscess, an infection of the brain. Here's something that many of you may not have heard of, but it's an important cause of seizures: a dysplasia. It is a nest of brain cells that during development got off at the "wrong elevator stop,"; they were supposed to migrate all the way out to the cortex, but in fact stayed deep in the brain. Brain cells in the wrong location are prone to cause seizures. At the right is an MRI of what everybody fears when they first have a seizure: a brain tumor causing seizures, in this case glioblastoma multiforme. In this case it is a malignant brain tumor, but benign brain tumors also cause seizures. Should someone you know have a seizure, there is a relatively small likelihood that it is from a brain tumor. Even if there is a brain tumor, it may not be a malignancy. I want to be careful not to scare the public into connecting seizure and brain tumors, they are not usually linked. The next task we have in the clinic is to choose a suitable medicine. We have about 20 medicines available. They have different profiles of side effects. Some people tolerate certain types of side effects better than others and some medicines work better for certain seizure types.

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We have a long history of medications for epilepsy, starting back in the 1850s. The first effective medication for epilepsy was bromides. Bromides came in at a time when it was thought that epilepsy is a form of insanity and insanity derived from abnormal sexual drive. So bromides and saltpeter were used to reduce the sexual drive. Saltpeter didn't do much, but the bromides actually turned out to be useful for treating epilepsy. In 1912 came phenobarbital, which was introduced as a long-acting sleeping pill, and also turned out to be useful for seizures. But it makes you sleepy and it can induce depression . In the United States and in most developed countries, it is a somewhat outdated medication, yet, it is the only medication that can be afforded in the developing world, where 70 to 80% of people with epilepsy can't get any medication at all. Here in the United States we are arguing over subtleties of which medications to use, but sadly in most of the world it is not possible for them to get any medications. Phenytoin or Dilantin (every medicine has a brand name and a generic name) is a medicine that was discovered by research into brain mechanisms and it has led to many others that I will not mention by name. On the right of the chart are medications on the launching pad. The length of this list, highlighted by the few that may be released within the next year, reflects a hope that the research community and pharmaceutical industry will not give up on looking for epilepsy medications, because even though two out of three people are satisfied with the medicines, one out of three, a very large number, are not and better treatments are needed. I'm familiar with most of these drugs, at least in prototype form, and there is no magic bullet that will displace all the other medicines. But having more of a choice of medicines is going to be useful. What we ultimately want is not a medicine to suppress seizures and make brain cells fire less quickly, but we would like a medicine to cure epilepsy. People could take it like an antibiotic for pneumonia, and then not have epilepsy anymore. People don't have to keep taking an anti-

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pneumonia pill. That's one of the holy Grail's in epilepsy: to learn what we can do to prevent or cure the epilepsy medically, instead of just giving a medication every day of a person's life to suppress the seizures and make them suffer whatever side effects occur as a consequence of those seizures. Much of what I do in clinic is balance seizures and side effects. If people are still having a lot of seizures and few side effects, we will increase medicine. If seizures are controlled and there are side effects, we will go the other way and decrease medicines. All too often, at least in a referral practice, there are both side effects and seizures, and then we need to consider another strategy, for example, a change in medications, or a streamlining because often people accumulate many medicines. Or we need to consider non-medical therapies. We want complete seizure control with minimal or no toxicity. In my view, many physicians set the bar too low. A person will come in and say "I've had three seizures this month." The doc will say "well did you fall and hurt yourself? No, then that's pretty good." It shouldn't be that way. The goal should be no seizures and no side effects. It may not always be possible to get there, but we should never be satisfied until we have tried. We should consider non-medical therapies, as well as the usual medicines. Non-medical therapies are several. One is brain surgery, which we will discuss in a minute. Another is a special diet, called the ketogenic diet. It derived from attempts to cure epilepsy by fasting and prayer. I shan't speak to whether or not the prayer worked, but the fasting did. It's just that you can't fast long-term. In the 1930s, it was discovered that it was not necessary to fast. It was just necessary to eliminate carbohydrates, and eat a very high-protein and high-fat diet. This generates ketone bodies, which the brain consumes as an energy supply instead of the missing glucose. That changes the chemistry of the brain in a way that makes it harder to have seizures.The ketogenic diet is not a miracle cure, but it improves seizures in some people. From the 1940s on, came many new seizure medicines, such as Dilantin, Tegretol, Depakote and so on, and the ketogenic diet fell by the wayside. Dr. John Freeman at Johns Hopkins and a few colleagues resurrected the ketogenic diet when medications were not working. It can be helpful, but it is not a cure. It is a high-fat diet, similar to the Atkins Diet, so it can have some health consequences. There are electrical stimulation methods for epilepsy, which we will discuss later. Relaxation or biofeedback is where you train yourself or use a feedback machine to help you learn behavioral states that keep you from having seizures. It occasionally is effective. Alternative therapies are used as well. In California about a third of people who come to our clinics are taking some type of complementary / alternative therapy. They may not tell the physician about these treatments unless we ask. It is important to ask, because some of the alternative therapies, whether they work or not, are drugs and may have interactions with the other treatments. Unfortunately, I cannot often tell them to what extent complementary/alternative therapies are effective or dangerous because evidence is lacking. Let me move now to epilepsy surgery. This skull, from a museum in Berlin, marks one of the first epilepsy surgeries ever done. It shows a trephine hole probably drilled to let out demons producing seizures or perhaps headaches. When I showed this in one talk someone asked me if the surgery worked and I said this patient has not had seizures for thousands of years, which is more effective than anything I have ever done. This is the largest operation that you will see for epilepsy. This is a hemispherectomy. This means that approximately half the brain is removed to stop seizures. It is an operation

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that's quite effective for someone who has very damaged half of the brain that is causing a great deal of trouble. You can imagine we don't do this too often. I recall one circumstance where we requested permission and insurance clearance for a hemispherectomy and the insurance company came back with a letter saying that they were going to give permission, but they wanted us to know up front that they were only going to approve one for this patient. They didn't want us coming back asking for another one if this one didn't work. Most operations are much more limited. You can see the thumb tip as a marker of size. This operation is called a partial temporal lobectomy. The temporal lobes on the side of the brain are the most seizure-prone parts of brain and this is the site which is most often operated on to cure epilepsy. A piece is removed about the size of a squashed golf ball, including deep structures, amygdala which is Greek for almond, and hippocampus, which is Greek for seahorse, which it rather looks like in anatomical crosssection. Hippocampus is involved in memory processes, and amygdala in emotionality. You can imagine there could be some price to be paid taking the structures out. However, if your hippocampus, amygdala and surrounding structures are damaged, and they are giving rise to seizures that invade the healthy adjacent brain, many people feel smarter and sharper after successful surgery. This is even more true if seizure control allows a reduction in medications. When seizures arise from critical areas of brain, including motor, skin sensation, speech, or comprehension regions, then we are much less likely to operate in those regions. Seizure surgery can be beneficial in cases where the seizures seriously interfere with the quality of life, and medications cannot control the seizures. Some people are not much bothered by seizures, and then it doesn't make sense to do surgery. Someone once said we only use 10% of our brain. That is nonsense all our brain is good for something. However, we know from experience that some parts are safe to remove and there are other parts are not. When people have intractable, uncontrolled seizures, our hope is that their seizures come from one place in the place in the brain, and that area is one of those that an safely be removed. Being a candidate for seizure surgery does not mean you need to have surgery: it is an elective procedure.

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When the seizures seem to be coming very close to a critical area of the brain, for example a speech comprehension area of the brain, then we need to give the surgeon a road map. In a

surgical procedure under general anesthesia, we will put a plastic grid (sheet) of electrodes on the surface of the brain. The contact points in the grid will determine in great detail where the seizure activity originates. It will also allow us to deliver brief pulses of electrical stimulation to see stimulation interrupts talking, wiggling fingers or any other functions that we may wish to map. Here's how a real grid looks on a real brain. That grid will let us draw the map to say it is safe to go here, it is important to go here to get out the seizure onset region, but you must keep away from this area. On the second operation, when the grid is taken out - usually about a week after the first - the brain that gives rise to the seizure is also removed. Most people with epilepsy don't need surgery and most people with epilepsy surgery don't need grid mapping, but it is something that is available and allows us to operate in otherwise difficult cases. I wish I could tell you that epilepsy surgery cures 99% of people, but it cures about 60% of people. In a randomized trial for a year comparing surgery to medication therapy, there was only one death, and it was, sad to say, in the medical group, not the surgical group. New treatments are being developed. This picture is of the Cyber-Knife device, invented here at Stanford by Dr. John Adler. It is computer-controlled mobile radiation source. An operator paints the targets to be radiated on a patient's MRI scan and the device swings around the head delivering radiation almost exclusively to the target. It is surgery without cutting even the hair.

This is vagus nerve stimulation, an electrical type of stimulation device that's implanted into the chest and connected to a nerve in the neck. That nerve feeds into the brainstem and changes the electrical activity in a way that makes it harder to have a seizure. It sounds Buck Rogers, but it works. This has been found effective in controlled

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trials. Vagus nerve stimulation is approved by insurance companies, and we use it. We don't use it in everyone because it's not likely to cure epilepsy. But it is safer than is brain surgery for epilepsy. We are putting stimulating electrodes directly into people's brains. I'm involved in a protocol testing brain stimulation in a deep structure here called the thalamus. You can see four electrical contacts in the thalamus. The deep brain stimulators are currently under testing. Note added. A recent study (called SANTE) has shown effectiveness of stimulating a part of the brain called the thalamus for partial and secondarily generalized seizures. Last but not least is helping the patient and the family about psychosocial seizures. My young students are concerned about seizure control. My better and more experienced students are concerned about the quality of life. Some seizures ruin the quality of life; other seizures are not that bad and it is actually the treatments for them that is ruining the quality of life. So this is the key thing. We have to treat the person and not the seizures. We have to consider issues of school, employment, marriage, having kids, employment and epilepsy, restrictions that exist on such things as driving and sports and activities. In the work arena, it is illegal to discriminate against people with epilepsy or any disability, but it's done all the time and it's very hard to prove. Sure, there are some things that people with epilepsy can't do. They can't be airline pilots and that's reasonable. But to discharge a salesperson because it's upsetting for the customers to see them have a seizure - that's not reasonable. There is considerable job place discrimination against people with epilepsy.. People who have uncontrolled seizures should not drive. This is a real car from a real patient who had a seizure. But people whose seizures are controlled may be allowed to drive. Every state regulates this separately in the United States, typically requiring either three, six or twelve months before someone can drive, after having a seizure. I'll close with some old remedies for epilepsy from a book by Temkin called "On the Falling Sickness." Lichen of horses - whatever that is, genitals of seals and hippopotamus testicles ,blood of the tortoise, discarded skin of the lizard, feces of a crocodile and a reasonably hard to obtain blood of the recently stabbed gladiator. My hope is that the treatments that we are talking about here will not appear on somebody else's version of this slide 50 years from now. One of the keys, as I said earlier, to solving the problem of uncontrolled epilepsy is research. Research takes support. It takes funding. The funding engine has been for the most part the National Institutes of Health and to lesser extent various foundations: the Epilepsy Therapy Project, CURE, the American

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Epilepsy Society and the Epilepsy Foundation. These days, only 8 or 9% of the would-be research applications are being funded, compared with 30 or 35% just a few years ago, because federal money has been going elsewhere. So if any of you who are listening know of any way to improve funding for research in epilepsy, please let us know. Epilepsy is a condition much more common, than say, muscular dystrophy, but epilepsy has no Jerry Lewis and no easy way to raise money. I will leave you with my favorite fortune cookie: Money spent on the brain is never spent in vain from Uncle Lees House of Szechuan in Baltimore, Maryland. Thank you very much.

Questions
First Aid: The question is whether people are still putting in tongue blades when people are having seizures. I hope not, because that's not the right thing to do. The correct first-aid procedure is to keep someone safe, and not to yourself panic. Put a coat or something soft under their heads. We recommend turning a seizing person on their side so the saliva does not run down into the lungs and produce what is called an aspiration pneumonia. Put nothing in the mouth. It's too likely that you'll break a person's teeth or have them inhale the object or you might get bitten. There have been too many mishaps. Only if you are a trained to use a soft oral airway should you put something in the mouth. Look at your watch. A minute seems like an hour to someone watching a seizure. If a seizure goes on for longer than five minutes without counting the wake-up time, then call 911. A long seizure: The question is about an 89-year-old father who had a complex partial seizure that went on for a long time. I'm not sure if it was one continuous seizure or one seizure that stopped and went into another one without full recovery. Yes, that would be a situation that should be treated at hospital and with some intensity. The seizure probably didn't harm the brain because it was partial and not as widespread as a grand mal seizure, although some people are rather confused for a while after seizure goes on that long and it requires some recovery. Epilepsy is not just something that happens in kids. It happens to people of any age. In fact, among seniors, there is a second peak in incidence that occurs where it is very common for someone 75 years of age to have a first seizure. Do seizures harm the brain? Seizures make brain cells all fire all at once in an abnormal synchronous activity. The normal activity of the brain involves a lot of independent chatter among brain cells. It's the analogy of a sports stadium before the team comes, when everybody's is talking with their neighbors: that's normal activity. The seizure is the wave or the cheer after a touchdown, where its almost impossible to do anything else because of that synchronous activity. When that wave passes, the nerve cells go back to normal activity again. If the brain exhausts its energy and people seem to be turning blue and not breathing during a seizure, the seizure usually dies down because a seizure requires oxygen. Then we automatically start breathing when the breathing centers take over again. People usually survive seizures very well. The most practical problem that I've seen is much more subtle. People who have uncontrolled seizures for years develop worse memory. The memory loss is not losing discrete of the past because the distant past is usually well preserved. It's what they had for lunch that they cant remember. Migraine: Is there a relation to migraine, such as ocular migraine, which is an eye-related migraines. They are two separate conditions. The most common link is that both are common and some people are so unfortunate as to have both. The next most common link is that some people have migraines after a seizure. The third link, which is extremely rare and I see only a couple of times a year, is someone who has a migraine so severe that it actually provokes an epileptic seizure. Sleep-walking: Is there any connection between seizures and sleep-walking. Sleep-walking is a sleep disorder and it does not usually result from seizures. Sleep-walking can be one of the imitators of epilepsy. The place where it might become confusing is where somebody has a

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complex partial seizure during sleep and then was befuddled and wandering in the aftermath. You should be able to tell the difference because a person can be awakened to normal from sleep-walking. Kindlilng and brain cell loss: These are two interesting scientific questions that we could talk about a long time. I'll give a short answer. The question was made about kindling. Kindling is a laboratory model of epilepsy by which brain stimulation is given day after day and eventually produces a seizure focus. That part of the brain has maladaptively learned how to have seizures. Its used in the laboratory where we make models to study epilepsy. Epilepsy specialists debate whether or not kindling happens in people. It probably can happen. Probably, it doesn't happen very often or epilepsy surgery would never work because the seizure focus that we take out to cure the epilepsy would over the years have kindled foci in other parts of the brain that would live on. Usually that does not happen. The second question was about brain cells constantly dying and renewing themselves. How I wish that were so! For the most part, you have all the brain cells you are ever going to have when you were born, and you just lose them. But there are two slightly hopeful statements against that bleak background. There are a few places in the brain, and hippocampus is one, that can make new brain cells. This is new evidence. Second, the real business of the brain is not at the brain cells, but at the trillions and trillions of synapses, which are the connections among brain cells. And you can make new synapses and connections until the day you die at 99 years old. Yes, it is possible that the brain can reorganize to work its way around the seizure. There have been many cases that I've seen in my practice where seizures have improved because of nothing that I or any of the other doctors have done to stop them. We always hold that as a possibility. Memory: Can seizures affect the memory during a seizure, either during a seizure when the memory is terrible or in the wake of a seizure, when the memory is poor for many days. Can that be confused with dementia? Yes it can. Most experienced neurologists give a thought to this if they are seeing someone with a memory problem, particularly if it is acute. Pregnancy and breast-feeding: All of the seizure medications are potential teratogenic (birthdefect producing) drugs. The baseline birth defect rate in the United States for anyone is about 1 to 2%. For women with epilepsy on seizure medicines, it is between 5-10%, so the risk is higher. But if you want to be a glass half-full type, you can say there is still more than a 90% chance of having a normal baby even with the higher risk. It seems that the higher risk is due to the seizure medication, not just the epilepsy, because these drugs are used for a lot of other conditions besides epilepsy and when they are, studies have shown that the birth defects are there as well. So why dont we stop the medications when someone might become pregnant? Because seizures also pose risks to the mother and the baby. So we try to use the fewest number of medications at the lowest possible dose that will likely control the seizures. Some medications seem better than others. According to the pregnancy registries and preliminary data, there were more birth defects on valproic acid (Depakote) or phenobarbital than on some of the newer medications. You mentioned breast-feeding. The seizure medications do come out in the breast milk, but we think that the benefits of breast-feeding outweigh the risks of traces of medications in the breast milk. Is Depakote still used? Depakote is still a very much used and it is a very valuable treatment for epilepsy. It is perhaps the most powerful medicine against certain types of generalized seizures. As I just mentioned, I dont like to use it in women who are or might become pregnant, but it is still useful for generalized seizures. Do seizure medicines lower intelligence? It's a good question. There are a lot of studies and experience to show that seizure medications that slow brain cell firing can impair cognition and memory, not in all people, but in some. Some medicines are worse than others in that regard; for example, phenobarbital is a more mind-dulling medication than are most of the newer seizure

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medications. In all cases in adults that I know of, when the medication is stopped, people go back to their usual level of cognition and intelligence. It can be a different story, if medication is given either to a pregnant mother or to a very young child during the developing time of the brain. They has been evidence, for example a study in the New England Journal of Medicine, that the IQ can be permanently lowered by certain seizure medicines in the first few years of life. But for adults, the expectation is that thinking returns to normal when the medications are stopped. Speaking of stopping, we are getting a sign that we are out of time, but I will be happy to stick around to answer questions individually. Thank you very much.

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Monitoring safety aids test questions for Out Of the Shadows Video
1. Epilepsy occurs in approximately what percentage of the worlds population? A. 0.1% B. 1% C. 3% D. 5% E. 10% answer: B. 2. Status epilepticus refers to seizures that go on for how long without stopping? A. 30 seconds B. 1 minute C. 10 minutes D. 30 minutes E. One hour answer: D. 3. Which of the following can imitate seizures? A. Fainting episodes (syncope) B. Transient ischemic attacks (mini-strokes) C. Complicated migraine headaches D. Sleep disorders, such as narcolepsy E. Psychological episodes F. All of the above answer: F 4. The most important activity for diagnosis of epilepsy is A. The history B. The physical exam C. The electroencephalogram D. The MRI E. Blood tests answer: A 5. An interictal (between seizure) spike on the EEG means A. The person is having a seizure at that moment B. brain cells have died C. Seizures will not respond to medicines D. Seizures are of a generalized type E. a higher risk for having epilepsy answer: E. 6. A patient has a seizure with the following description. It starts with an upset stomach sensation, then difficulty saying words, fumbling of the hands and inability to remember what happened for about one minute. This seizure type most likely is: A. Simple partial B. Complex partial C. Generalized tonic-clonic D. Atonic E. Myoclonic answer: B. 7. A patient stiffens, loses consciousness immediately, falls to the ground and begins jerking. The event lasts two minutes and recovers over another five. The most likely seizure type is: A. Simple partial

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B. Complex partial C. Generalized tonic-clonic D. Atonic E. Myoclonic answer: C. 8. A six-year-old boy has episodes in which he suddenly becomes limp, falls to the ground and lies they are without any movements. He recovers over a few seconds. The most likely seizure type is: A. Simple partial B. Complex partial C. Generalized tonic-clonic D. Atonic E. Myoclonic answer: D. 9. All of the following, except one, are possible causes for seizures. Which one is least likely as a seizure cause? A. Head trauma B. Muscular dystrophy C. Brain abscess D. Birth defect in brain, such as dysplasia E. Stroke answer: B. 10. Which is a true statement about antiepileptic medications? A. Most of them cure epilepsy B. They have very few side effects C. They stop all seizures in over 90% of patients with epilepsy D. New ones are unlikely to be invented E. Taking them can make seizures less likely to occur answer: E. 11. Which is a true statement about epilepsy surgery? A. It is elective, meaning a matter of patient choice. B. It is most effective when done on both sides of the brain C. Surgery eliminates all seizures in over 95% of cases D. The frontal lobe is the most common place to have epilepsy surgery E. Mortality of epilepsy surgery is approximately 20% Answer: A. 12. All but which one of the following is used as a current medical treatment for epilepsy? A. Vagus nerve stimulation B. Ketogenic diet C. Medications D. Exorcism of demons E. Brain surgery answer: D. 13. True or false: People with uncontrolled seizures should not drive. A. True B. False answer: A.

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ANSWERS
1. B. 2. D. 3. F 4. A 5. E. 6. B. 7. C. 8. D. 9. B. 10. E. 11. A. 12. D. 13. A.

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SHORT VIDEO SEGMENTS B. Different types of seizures 01. UNDERSTANDING EPILEPSY

A seizure is a symptom of many different disorders that can affect the brain, not a disease in itself. In centuries past, the word "seizure" referred to people being taken over by supernatural forces.

Today, we understand that a seizure is not a supernatural entity. It is simply a medical condition in which too many brain cells become excited at the same time. The brain is an electrochemical machine Nerve cells or "neurons" use chemical reactions to generate electricity, like a very complex battery.

When a neuron becomes excited, it passes an electrical signal along its thin biological wire, called an axon, to communicate with other neurons in the brain. Those other neurons either can be excited or inhibited by the signal. If too many neurons become excited all at once then a seizure can result. So a seizure is like an electrical storm. During this abnormal electrical storm, involved parts of the brain cannot perform their normal tasks and people experience sudden alterations of movements, sensations awareness or behavior . A seizure typically goes on for a few seconds to a few minutes. The end of a seizure is a transition back to the individual's normal state. Because the word "ictus" is Latin for "seizure," this period of recovery is referred to as the "postictal" period, which can last from seconds to hours. A person's level of awareness gradually improves during the postictal period. Doctors often are asked what the difference is between seizures and epilepsy. To the medical community, epilepsy is the condition of having spontaneously recurrent seizures.

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That means that one isolated seizure is not defined as epilepsy. There must be two more seizures, or at least one seizure with a high chance of having another. To count as epilepsy, seizures have to appear spontaneously, without an immediate precipitating factor. For example, if Johnny falls off his motorcycle, hits his head and has two seizures on the scene, it is not epilepsy because the seizures were immediately precipitated by head trauma. However, if he recovers and starts having seizures weeks, months or years later as a result of a traumatic brain injury, then that does count as epilepsy. Epilepsy has a long history of social stigma, but epilepsy is nothing more than a brain disorder caused by uncontrolled excessive and synchronous electrical activity. If you are concerned that you might have epilepsy, see a physician.

02. TYPES OF SEIZURES

The word seizure is a general term used to describe the medical condition in which too many brain cells become excited simultaneously.

There are so many kinds of seizures that neurologist are still updating how to classify them. Usually, they classify seizures into two main types: partial seizures and primarily generalized seizures. The difference between these types is in how they begin. Primarily generalized seizures begin with a widespread electrical discharges that involve both sides of the brain at once

. On the other hand, partial seizures begin with electrical seizures in one limited area of the brain. All generalized seizures begin with synchronous electrical activity throughout the brain, accompanied by sudden generalized movements or loss of consciousness. However, there are still many different types of generalized seizures.

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A tonic-clonic seizure, once called grand mal, is what most people think of when they hear the word seizure. When someone experiences a tonic-clonic seizure, first they stiffen and lose consciousness, which is the tonic phase. Then they begin jerking and this lasts for several minutes, called the clonic phase. Sometimes, seizures don't have a tonic stiffening and a clonic jerking sequence, but are just tonic seizures or clonic seizures. Other types of generalized seizures include absence seizures, when the sufferer disconnects from the world for a few seconds, and myoclonic seizures which cause jerking, but just for a second or two. Partial seizures, which began in a single part of the brain, are further described by two important additional criteria. The first is whether awareness, memory and consciousness are preserved during the seizure. If they all are preserved, then the seizure is called simple partial. However, if any are impaired, then the seizure is called complex partial. The impact of a partial seizure depends on where in the brain it originates and how it spreads. Partial seizures sometimes have an aura, which is a warning that bigger seizures may follow. An aura usually occurs seconds to minutes before a seizure. But some patients can have periods of warning lasting a day or longer. There are many different ways in which people experience an aura. The start of a seizure in one of the temporal lobes can produce unusual feelings, abnormal sensations, or forced thinking. The onset of a complex partial seizure may be heralded by dj vu, a familiar feeling, or jaimais vu, an unfamiliar feeling. Some patients have auras of sounds, tastes, distorted vision, racing thoughts or smells, like burning rubber. Physical sensations that can occur as auras include dizziness, headache, lightheadedness and numbness. An upset stomach is a particularly common physical symptom. Auras can include a sense of tingling rising up the body or other strange feelings that are difficult to describe. Distorted emotions, like fear or panic, can also be a seizure warning; however, some complex partial seizures occur without any remembered warning. Understanding the different types of seizures can be helpful, but many people want more detailed information. The next two videos in this series provide an in-depth look on the effect of partial seizures on different parts of the brain and the different types of generalized seizures. If you or anyone you know may have seizures, please make sure that they see a physician.

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03. UNDERSTANDING PARTIAL SEIZURES

Partial seizures, which involve an electrical discharge in a limited area of the brain, come in a variety of forms. Let's look at some common types. A partial seizure begins with an electrical discharge in one limited area of the brain. How a partial seizure affects someone depends upon whether it is a simple partial seizure or complex partial seizure, and where in the brain it occurs.

Different parts of the brain control different functions. The cortex or thinking part of the brain is divided into four lobes: frontal, temporal, parietal and occipital. Other deeper brain structures relate to life-support functions, movement and other semiautomatic behaviors. At the back end of the frontal lobe is the motor strip, which signals muscles to move. A seizure in this part of brain will cause uncontrolled movements or twitching lasting for a few seconds to a few minutes.

Towards the top of the motor strip are nerves controlling the leg muscles. Lower down are nerves controlling the trunk, then the arms, fingers, face and mouth. If the seizure spreads along the motor strip, then the seizure can march along different parts of the body. Just behind the motor strip is the skin sensation area. A seizure here will cause tingling in the affected part of the body; however, tingling in the skin usually is not due to seizures. The back lobe of the brain is the occipital lobe. It contains brain cells responsible for vision. Seizures in the occipital lobe can produce flashing lights, shimmering lines or visual hallucinations. The temporal lobe is the part of the brain most prone to develop

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seizures. It is responsible for many complex activities, including the formation and retrieval of memories and the control of emotional states. If a temporal lobe seizure spreads to both temporal regions, then the manifestations of the seizure increase, with a pause in ongoing activities, confusion, temporary memory loss and fragmentary automatic "robot-like" behaviors. This type of seizure is called a complex partial seizure. It is the most common type of seizure in adults. In general, when awareness, memory and consciousness are preserved, then the seizure is called "simple partial." However, if any are impaired, then a seizure is called "complex partial." Someone experiencing a complex partial seizure lives in a moment-to-moment world. During this time, he or she may repeat the same phrase or action over and over in an automatic loop, not recognizing the repetition. This person also may fumble hands, smacked the lips, or grab tightly onto things during a seizure. This automatic activity is called an automatism. Others just freeze in place and stare blankly, with no automatisms and hardly any movement. After a complex partial seizure, people dont remember what was said or even what they did during a seizure. Some don't remember having a seizure at all. Later, the memory starts working again, except for a gap during a seizure. Understanding what occurs during a seizure begins with the insight that there are different kinds of seizures, each with a different impact. If you, or someone close to you, is suffering from seizures, please see a physician.

04. UNDERSTANDING GENERALIZED SEIZURES

Generalized seizures, which involve a widespread electrical discharge across both sides of the brain, come in a variety of forms. Let's look at some common types. Generalized seizures are characterized by synchronous electrical activity throughout the brain. But each type of generalized seizure has a different effect on people. Here's a typical story from the parent of someone who gets tonic-clonic seizures, which were once called grand mal seizures: "These seizures only last a minute or two but it seems like forever. It begins with an unnatural shriek and she falls and every muscle seems to be activated. Her teeth clench. Shortly after she falls, her arms and upper body start jerking while her legs remains stiff. Finally it stops and she falls fast asleep".

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A tonic-clonic seizure is what most people think of when they hear the word seizure. Although these seizures are distressing to watch, the person having them is unaware. We don't believe that the seizures are painful, but people can injure themselves by biting their tongue or straining their muscles. The tonic or stiffening phase comes first. All the muscles stiffen. Air being forced past the vocal cords causes a cry or a groan. The person loses consciousness and falls down. The tongue or cheek may be bitten, so blood or saliva may emerge from the mouth. The person may turn blue in the face. After the tonic phase, comes the clonic or jerking phase. The arms or legs jerk rapidly, bending and relaxing. After a few minutes, the jerking slows and stops. Bladder or bowel control sometimes is lost as the body relaxes, leading to incontinence. Consciousness returns slowly and the person may be drowsy, confused, agitated or depressed. Sometimes, seizures dont have tonic stiffening and clonic jerking sequences, but are tonic only or clonic only. Absence seizures used to be called petit mal seizures. Here's a typical story: Frank, a young man, often blanks out for up to 20 seconds at a time. During a seizure, Frank doesn't seem to hear anyone. He blinks repetitively and his eyes roll up a bit. During shorter seizures, he just stares. Then he continues, as if nothing happened. Some days, Frank has over 50 of these spells. Absence seizures usually begin between ages 4 and 14. They can resemble episodes of daydreaming. If they go on for more than 30 seconds or if there is a lot of movement, then the seizure is called an atypical absence, which is harder to treat. Here's a story from someone who gets myoclonic seizures: "Each morning, I get these jumps. My arms fly up for a second and I often drop what I am holding. Sometimes, my mouth shut for a split second. Once I am up for a few hours, the jumps stop." Myoclonic seizures usually last only a second or two. It can be just one jerk or a series of several. Consciousness may be lost, but seizures usually are so brief that it is hard to tell.

Here's a typical story from someone whose husband has atonic seizures: "When Bob has a drop seizure, he falls to the ground and often hits his head and bruises himself. Even if I'm right next to him and prepared, I may not catch him." A sudden loss of muscle tone during an atonic seizure can cause the head to drop suddenly, objects to fall from the hands or the legs to lose strength. This type of seizure is also called an akinetic seizure or an epileptic drop attack. If you have or think you may have one of these types of epileptic seizures, please see a doctor.

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C. Diagnosing Epilepsy 05. WHAT CAUSES EPILEPSY

Epilepsy affects nearly 3 million Americans, but who is really at risk? Epilepsy can develop in any person at any age. Almost 1% of people will develop epilepsy during their lifetime. That's 60 million people worldwide. In other words, out of a 60,000 person stadium, about 500 will have epilepsy. New cases of epilepsy are most common among children, especially during the first year. The rate of new cases gradually declines until about age 10 and then become stable. After age 60, the rate starts to increase again. Many famous people in history had or may have had epilepsy, including world leaders like Julius Caesar, writers like Lewis Carroll who wrote Alice in Wonderland, artists like Vincent van Gogh, and athletes like Chanda Gunn, goaltender for the US Olympic hockey team. The causes of epilepsy can be divided into two groups: brain injuries and chemical imbalances in the brain. Anything that injures the brain can lead to seizures. But in over half the cases no cause can be identified. The type of injury that can lead to a seizure is age-dependent. Seizures in children often are caused by birth traumas, infections, such as meningitis, congenital abnormalities or high fevers. Seizures in the middle years commonly are caused by head injuries, infections, alcohol, stimulant drugs or medication side effects. In the elderly, brain tumors and strokes cause a higher proportion of seizures. Not all seizures result from a structural problem in the brain. Chemical imbalances also can cause seizures. Common chemical imbalances that can produce seizures include drugs like alcohol, cocaine and others, low

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blood sugar, low oxygen, low blood sodium or low blood calcium. Kidney failure or liver failure can also produce seizures. Doctors will evaluate you for these imbalances by taking a careful history and doing blood tests. Although these disorders and injuries can explain many cases of epilepsy, often the cause of epilepsy remains idiopathic, which is the medical term for unknown. About half the time no cause for seizure can be identified. Fortunately, we do not need to know the cause to treat the seizures. Scientists increasingly recognize the importance of genetic factors in the origin of epilepsy. Genetics or heredity are most relevant to generalized seizures, including absence, generalized tonic-clonic and myoclonic seizures. Defects in genes don't directly lead to epilepsy, but they can alter the excitability of brain in a way to predispose to the seizures. Typically, epilepsy develops because of multiple gene abnormalities or because of a gene abnormality in concert with an environmental trigger. Parents with epilepsy wonder whether their children will have epilepsy. In most cases they won't, but they do have a higher risk than others. If the mother has a generalized type of epilepsy, then the child's chance of having epilepsy may be as high as 5-20%. But if a parent has epilepsy due to a brain injury, the child's chance of having epilepsy is only about 5%. If you or someone close to you is suffering from seizures, please see a physician.

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06. HOW IS EPILEPSY DIAGNOSED?

Seizures can be confused with the symptoms of a number of other conditions. For this reason, doctors rely upon four distinct methods to diagnose epilepsy.

To make a proper diagnosis of epilepsy, doctors use four methods: history, exam, EEG and MRI. The first method used to make a diagnosis of epilepsy is the neurological history, when the doctor is given a clear description of any past seizure activity. Most seizures have a clear start and finish, last from seconds to a few minutes, occur at seemingly random times and comprise certain sensations and behaviors that clinicians can recognize. Patients may not remember their behavior during seizures, so descriptions from observers are very important.

The second method used to diagnose epilepsy is the physical exam. A physical exam cannot uncover epilepsy, but it can show problems indicating that a part of the brain isn't working properly and therefore may be generating seizures.

The third method of diagnosis is an EEG or electroencephalogram, which measures the patient's brain waves. The brain produces electricity, which can be measured by wires glued onto the scalp. The EEG records and charts these electrical voltages. The normal upand-down movements of the voltages create the wave-like patterns seen here. Spikes on the EEG are markers of hyper-excitable

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parts of the brain, which mark potential locations where seizures may arise. The presence of spikes helps to confirm a diagnosis of epilepsy, provided the history is also convincing. Some people have EEG spikes without seizures, so a history of seizures is needed to make a diagnosis. The fourth method to diagnose epilepsy is neuroimaging. Neuroimaging looks at the structure of the brain. The two most commonly used neuroimaging tests are a brain CT scan and a brain MRI. A CT is faster, easier and less expensive, but an MRI shows more detail. Neuroimaging cannot show abnormal electrical activity or a seizure itself, but may show physical changes in the brain which may suggest a reason for seizures. This MRI shows bruising of both frontal lobes in a case of head trauma, although head trauma without loss of consciousness rarely causes epilepsy. Serious head trauma with prolonged loss of consciousness sometimes does. People with seizures worry that they might have a brain tumor, like the one seen in this MRI. But fortunately, brain tumors only cause a small percentage of seizures. This MRI shows a region of stroke, which results from a sudden blockage of blood flow to the brain. Seizures don't cause strokes, but strokes can lead to seizures when brain cells are injured and can no longer control their electrical activity. One stroke can cause ongoing seizures for years. Abnormal blood vessels in the brain, such as aneurysms, arteriovenous malformations or cavernous angiomas can all cause seizures. The malformation itself does not generate seizures, but the irritated brain cells nearby may. This is a congenital abnormality of the brain called a dysplasia or a birthmark in the brain. A dysplasia is made up of normal cells in an abnormal location. Dysplasias don't grow, but they are a common cause of epilepsy. Your doctor will combine information from your history, exam, and if needed, EEG and MRI to determine if you have epilepsy. A diagnosis cannot always be made, but if diagnosis is difficult, you can be referred to an epilepsy specialist for a more detailed evaluation.

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The Burden of Epilepsy 07. TEN TRUTHS ABOUT EPILEPSY

Although epilepsy has affected people for millions of years, myths about the disorder still abound. Let's look at some basic facts about epilepsy. Up to 60 million people in the world currently have epilepsy, a neurological condition that affects the nervous system. Epilepsy is a condition of recurrent seizures. A seizure is a sudden, excessive discharge of electrical activity in the nervous system that causes a change in behavior, movement, sensation or consciousness. Because epilepsy varies from person to person, it can be helpful to examine some critical facts about the condition. Let's look at ten of them. 1. People with epilepsy should not be called "epileptics," as this term defines someone by one trait only. It is better to use the term "a person with epilepsy." To many, the term "seizure disorder" is also synonymous with epilepsy. 2. Another truth about epilepsy is that people with the condition are seldom brain damaged. While brain function can be temporarily disturbed by seizures, brain damage or a permanent problem with the brain structure is not synonymous with epilepsy. 3. Like any other group, people with epilepsy have different intellectual abilities. Some are brilliant, while other have problems with basic cognitive functioning. For the most part, though, people with epilepsy have normal intelligence. 4. Although seizures can be confusing and are often misconstrued as violent or challenging behavior, people with epilepsy have no greater tendency toward violence or aggression than do others. 5. Despite ancient falsehood that put epilepsy in the same class as mental illness, one has nothing to do with the other. 6. Single seizures that last less than ten minutes are not known to cause brain damage or injury in the long-term. While there may be a cumulative effect from frequent seizures, this appears to be rare. 7. Another fact about epilepsy is that the condition is not usually inherited. While some types of epilepsy are passed on through family, the majority of cases have unknown or environmental causes. 8. Most people who develop epilepsy have seizures and require medication for only a small portion of their lives. In fact, about 60% of people find that it goes way with treatment.

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9. Witch hunting in the 1490s focused on finding people with seizures and even the Bible declares that epilepsy is caused by an internal devil. Contrary to these stigmas, however, epilepsy is a medical problem and nothing more.

10. Perhaps the most liberating truth surrounding epilepsy is that it is perfectly compatible with a normal happy life. A positive outlook, a supportive environment and good medical care usually make it possible to live fruitfully with epilepsy. Although epilepsy has generated fear and confusion in the past, modern medicine has been able to break down many of the myths about this common condition. Remember, if you think you may have epilepsy, please see your doctor.

08. EPILEPSY THROUGH THE AGES

Epilepsy has attracted attention and been a source of controversy throughout the ages. Let's look back at the history of this condition.

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1% of the world's population has epilepsy, a condition of spontaneously recurrent seizures. A seizure is a sudden, excessive discharge of nervous system electrical activity that usually causes unexpected changes in behavior, motor function, sensation or consciousness.

Epilepsy is not a new affliction. In fact, the esteemed Greek physician Hippocrates wrote the first book on epilepsy in 400 BC. Hippocrates refuted the idea that epilepsy was a curse or a sign from the gods. In 70 A.D., epilepsy even made a debut in the Bible. In the Gospel according to Mark, Jesus Christ casts a devil from a boy with seizures. Years later, in 1494 two Dominican Friars wrote a handbook which identified seizures as a

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characteristic of witches. The persecution that followed resulted in over 200,000 deaths (erratum: up to 100,000 may be a more accurate number). Epilepsy continued to be a condition of confusion and controversy when in the mid1800s, three English neurologists ushered in the modern era of epilepsy. At this time, one of the neurologists, John Hughlings Jackson, defined a seizure as "an occasional, excessive and disorderly discharge of nerve tissue on the muscles." From Jackson and others, epilepsy was declared to come from the brain. Several years later, in 1904, the American William Spratling coined the term epileptologist, a doctor who specializes in epilepsy. In 1912, the first seizure medication, phenobarbital, was created as a sedative, but it soon was found useful for seizures and it is still used today. Eight years later the ketogenic diet was devised. This meal plan is high in fat and proteins. It is meant to simulate the effects of fasting, a state that can decrease seizures. In 1929, the German psychiatrist, Hans Berger, invented the electroencephalogram or EEG recording method. This made it possible to record the brain's electrical currents without opening the skull. In the next 30 years, a host of new epilepsy medications were introduced to treat and prevent the range of seizures. In 1909, the International League against Epilepsy was founded, and in 1968 the Epilepsy Foundation of America, along with the American Epilepsy Society, the Epilepsy Therapy Project, {the Klingenstein Foundation and the CURE Foundation} and particularly the National Institutes of Health. These are now the main organizations dedicated to fighting epilepsy. Even in the 20th century, some states had laws forbidding people with epilepsy to marry or have children. Luckily, this practice was ended with the Americans with Disabilities Act of 1990. During the next 10 years, new medications provided even more seizure control and in 1997, the FDA approved a device, the vagus nerve stimulator, to treat partial epilepsy in adults. It's clear that people with epilepsy have come a long way toward healing and society has come a long way toward understanding.

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D. Important Etiologies (Causes) of Epilepsy 09. GENETIC CAUSES OF EPILEPSY

Epilepsy can be caused by genetic factors or acquired, although in most cases it arises in part from both. In this video, we will look at the genetic causes of epilepsy.

First, some basics. What is a gene? Our genes are the instruction set for building the human body. Genes reside on chromosomes. Every person has 46 chromosomes, carrying a total of about 30,000 genes. We get half our chromosomes from our mother and half from our father. While genes determine the structure of our body, they also control the excitability of our brain cells. Defective genes can make hyperexcitable brain cells, which are prone to seizures. In recent years, several epilepsy conditions have been linked to mutations in genes, but the matter is complicated by the fact that different genes may be involved in different circumstances. In general, the most common epilepsy conditions, including partial seizures, seem to be more acquired than genetic. But even partial epilepsy has a genetic component. For example, if two people suffer a similar blow to the head, only one may develop epilepsy. This is because some people have genetically determined risk factors for developing seizures after head trauma.

Recently, doctors have discovered a technique called the gene chip, which can quickly screen thousands of genes in an individual. Each bright spot in the chip represents a strong presence of a particular gene in the person being tested. But how can knowledge of genes help us become more aware of epilepsy and better able to treat it? For example, genetic testing can help us to diagnose certain epilepsy conditions. Gene testing will soon be able to identify predispositions to epilepsy, allowing

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doctors to help a patient get treatment and to assist with family counseling. One day, doctors may simply be able to swap a patient's cheek, test his or her genes, and predict response to various epilepsy medicines, eliminating much of the trial and error in medication choice that goes on today. Eventually, we may even be able to repair or replace defective genes that predispose a person to epilepsy, a process called gene therapy. The general population has about a 1% risk of developing epilepsy. Meanwhile, children of mothers with epilepsy have a 3 to 9% risk, while children of fathers have a 1.5 to 3% risk. Still, the actual risk is upon the specific type of epilepsy. For example, partial seizures are less likely to run in families than are generalized seizures. In any event, with the usual forms of epilepsy, even if a parent does have the condition, there is more than a 90% chance that their child will not. Clearly, genes determine a great deal of who we are, including our risk for epilepsy. But what happens to us in life and what we do is still the larger part of the risk for epilepsy. Talk to your medical team and genetic counselors for more information about genetic predisposition to epilepsy.

10. FEBRILE SEIZURES

Febrile seizures occur in 3 to 5% of children ages six months to six years. A febrile seizure is a seizure that is provoked by fever above 100 F. A febrile seizure or even several febrile seizures does not point to epilepsy. This is because the seizures are not spontaneous and most children outgrow them by age 6. A febrile seizure is a very frightening experience for parents, partly because the fever may not be recognized until after the seizure occurs. In addition, the seizure often takes the form of a convulsion. Still, febrile seizures usually are harmless, unless the child is injured during a seizure. In fact, two studies of febrile seizures showed that the intellectual development of children was the same as their siblings who did not have seizures. Following the first febrile seizure, a child should be evaluated right away to rule out infectious meningitis and other serious causes of seizures and fever. Meningitis can be ruled out by a spinal tap or even with clinical observation. Febrile seizures do have a tendency to run in a family. For example, a younger

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sibling of a child with febrile seizures is three times more likely than normal to experience the condition. Even so, most febrile seizures occur with no family history of seizures. After one febrile seizure, about half of children will have another one sometimes in their life, but this does not necessarily lead to epilepsy. Several studies have examined the risk for later epilepsy in children with febrile seizures, and found it to be in the range of 2 to 4%. This means, in reverse, that 10 to 20% of people with epilepsy have previously had a febrile seizure. Certain complicating factors can increase the risk for later epilepsy after a febrile seizure. Among them are febrile seizures longer than 15 minutes, febrile seizures in one focal part of the body, multiple febrile seizures within 24 hours or a family history of non-febrile seizures. It is difficult to notice or treat arising fever before a febrile seizure occurs. Daily antiepileptic medications might prevent febrile seizures, but there is no good evidence that trying to prevent this condition with antiepileptic medications reduces the risk that a person later will develop epilepsy. This is an important issue, since seizure medications can impair a child's learning and personality. For example, phenobarbital, which is the usual medication used to prevent febrile seizures, can produce hyperactivity and behavioral and learning problems in a significant percentage of children. For these reasons, most pediatric neurologists believe that treatment of febrile seizures is worse than the risk of having one, and advise no therapy.

Remember, though 3 to 5% of children will experience febrile seizures, they are only a very slight risk marker for later epilepsy, as over 90% of the children with febrile seizures will not develop epilepsy.

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11. SEIZURES FROM STROKES

Strokes and seizures. Both can be very disturbing, but do they have anything else in common? People sometimes confuse strokes and seizures, but they are two very different conditions. First, here are some basics about each. A stroke results from reduced blood flow to all or some part of the brain, in turn leading to the death of some brain cells. Meanwhile, a seizure is the result of excessive, synchronous electrical activity in brain circuits. Eventually, a brain affected by a seizure will recover. A seizure may appear more dramatic and upsetting, but a stroke is medically much more serious because in stroke brain cells die. So how are strokes and seizures linked? First of all, strokes and seizures are common and some people can actually have both. Anything that injures the brain, including strokes, can lead later to seizures. In addition, strokes and transient ischemic attacks or TIAs,, which are sometimes called warning strokes, can be mistaken for seizures. A seizure also can imitate stroke. However, it is important to note that seizures almost never cause strokes. However, a body part that is involved in a seizure may be temporarily weak or paralyzed and this can look like a stroke. Temporary paralysis postseizure is called Todd's paresis. On rare occasions, about 2 to 5% of the time, a stroke will lead to one or more seizures. If seizures occur within a week of a stroke, then it is called an acute symptomatic seizure and is not diagnosed as being epilepsy. A seizure that occurs more than a week after a stroke does raise the question of possible epilepsy. Two more seizures post-stroke is definitely epilepsy. Some types of strokes are more likely than others to produce seizures, such as bleeding in the brain or a traveling blood clot called an embolus that blocks a brain artery. Epilepsy that follows a stroke sometimes can be delayed even months or years after the stroke. This may be because as circuits in the brain heal and reconnect over time, they become more hyper-excitable, making the brain more prone to seizures. Importantly, a seizure does not mean that the person is having another stroke.

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When epilepsy occurs later in life, it may stem from prior strokes, even very small ones of which the person is not aware. While scars from these small strokes may be visible on an MRI, there is no easy way to know which, if any, of the scars is causing the seizures. Treatment of seizures caused by strokes is similar to treatment of any partial seizure. It usually involves antiepileptic medications. Of course, preventing a future stroke is also very important. More information can be obtained from your doctor or by searching the web for stroke prevention information. If you or someone you care about maybe having seizures or stroke symptoms, please contact a physician.

12. SEIZURES FROM HEAD TRAUMA

Epilepsy can be a delayed consequence of head trauma. In fact, about 5% of all cases of epilepsy are due to this. Head trauma is very common in today's world. In addition to trauma from vehicle crashes and sporting accidents, head injury is becoming the signature injury of modern warfare. Over 1 million Americans sustain head trauma each year, but fortunately only a minority of these are severe. So how often does civilian head trauma lead to epilepsy? It generally depends upon how severe the head trauma is. Mild head trauma, with loss of consciousness for less than 30 minutes, is associated with barely increased risk of developing epilepsy compared to the general population. Severe head trauma can be defined as either loss of consciousness or amnesia for greater than a day or internal bleeding in or around the brain. Severe head trauma leads to epilepsy in about 15% of adults and about 30% of children. Injuries with actual penetration of the brain, like a bullet wound, are even more likely to cause epilepsy, about to 25 to 50% of the time. Studies have looked at whether treatment with seizure medicines immediately after trauma, before a seizures occur,

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prevents epilepsy, the condition of spontaneously recurrent seizures. Unfortunately, it does not. Medication simply suppresses seizures while the patient takes them. If a person does have a seizure post injury, a clinician will place it in one of two categories: early seizures, in the first week after an accident, or late seizures occurring more than a week after trauma. Only late seizures are considered to be epilepsy. Early seizures are a risk factor for later epilepsy, but most of the time they pass uneventfully. An early seizure may not require treatment, but a seizure or two occurring later would be treated by many doctors with the usual anti-seizure medications. Posttraumatic seizures may not appear for as long as 20 years after an accident. Laboratory studies suggest that this may be due to the long-term repair process after head injury. This repair process happens as new connections and circuits are formed in the brain over a period of years. While this aids recovery of strength, speech and memory, it may also form hyper-excitable circuits that are prone to seizures.

Head trauma can cause many problems in addition to seizures. People often develop migraine headaches, memory and concentration problems, dizziness, mood swings and various other symptoms known as the concussion syndrome. Even after seemingly minor trauma, these symptoms can persist for months. With more severe head trauma, neurological symptoms sometimes can be permanent. In conclusion, head trauma is common and usually mild, but severe head trauma can lead to epilepsy. There is a great need for a long-term medication that will prevent the development of epilepsy after trauma and other types of head injury, and research is currently being conducted to find one.

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E. Conditions that Imitate Seizures 13. SEIZURE IMITATORS OVERVIEW

Seizures can be scary, but they are often manageable once diagnosed. But what if what youre experiencing isn't really a seizure? Some medical conditions can cause symptoms that mimic certain aspects of seizures, which can make diagnosis difficult. These imitators can be grouped according to the characteristic of a seizure that they impersonate. They include movement imitators, loss of consciousness imitators, confusion imitators and psychological imitators. Each of these imitators may cause a symptom that looks like a seizure in some way, but they do not show the EEG changes in the brain that are characteristic of an epileptic seizure. Movement imitators of seizures often manifest as unusual postures or movements, including twitching or twisting. A well-known example of a movement imitator is a tic, which is a habitual quick movement that may be somewhat voluntary. Loss of consciousness imitators are conditions that may cause the patient to lose consciousness, which can be mistaken for a seizure. The most common reason for loss of consciousness, unrelated to seizures, is a faint. Fainting happens when the brain does not get enough blood flow for one of several possible reasons. Another category of seizure imitators are conditions that result in sudden confusion. This confusion may look like the uncertainty sometimes experienced by a person having a seizure. A transient ischemic attack or mini-stroke occurs when blood flow to the brain is briefly interrupted. If a transient ischemic attack affects the speech or memory centers in the brain, sudden bewilderment may result. Finally, psychological imitators are the group of imitators that are often the most difficult for doctors to distinguish from epileptic seizures. Psychological imitators include some common conditions, like hyperventilating. When a person hyperventilates, he or she is essentially breathing very fast. Hyperventilation often accompanies a panic attack, which

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is another common psychological imitator of seizures. But perhaps the most perplexing of all the psychological imitators are psychogenic nonepileptic seizures or PNES. A PNES is a seizure-like event, but it does not arise from abnormal discharges in the brain. Instead, a PNES is brought on by psychological factors. Most of the time, people who experience a PNES are not aware of the psychological conditions that cause them. In the end, so many conditions can imitate seizures that it is important to get a doctor's professional opinion. For a more in-depth look at seizure imitators, please check out the other videos in this series.

14. CONSCIOUSNESS IMITATORS OF SEIZURES

Several conditions can result in loss of consciousness, yet not be associated with the abnormal electrical discharge in the brain characteristic of a seizure. When a person suddenly loses consciousness, it can be a tense moment. If an observer reports that a person is stiffening, shaking or jerking during a period of unconsciousness, or of an experienced medical history taker notes symptoms of epilepsy, then the event can be categorized as a seizure. Often, however, this period of unconsciousness goes unobserved or the symptoms during the event are unclear. It is important to understand that there are other conditions that can cause loss of consciousness. The most common medical cause of loss of consciousness is fainting, for which the medical term is syncope. Fainting happens when the brain does not get enough blood flow. You can blame the fight-or-flight response for this occurrence. When the brain experiences a sudden stress, the blood rushes to the muscles in anticipation of fleeing or counterattacking a danger. The contraction of the muscles during the fight-or-flight that follows returns blood to the heart and brain. But in modern society, we may not react to certain kinds of perceived danger or pain, like the drawing of blood for laboratory tests. In cases like this, blood pools in the muscles and the lack of muscle contraction may prevent the heart from having enough blood to pump to the brain. This can cause the brain to temporarily shut down, resulting in vasovagal syncope, the medical term for a common faint.

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Fainting can also happen when people have lost blood, are dehydrated or have certain cardiac problems. Fainting from heart problems can be serious and requires immediate medical investigation. Usually when people faint, they lie limp. However, some faints provoke a true seizure, which is one way the brain may react to reduced blood supply. A seizure with fainting, which is called convulsive syncope, does not imply epilepsy, but it does require that medical professionals look into what is causing the fainting.

In other cases, loss of consciousness can stem from a loss of one of the brains two vital fuels: sugar and oxygen. Excessively low sugar is called hypoglycemia and can cause loss of consciousness. Low sugar can result from prolonged fasting, excess insulin hormone, medication side effects or a reaction to a high carbohydrate meal. People with hypoglycemia usually feel a build-up of hunger, lightheadedness and general ill feeling before losing consciousness. While hypoglycemia can cause symptoms like loss of consciousness that imitate seizures, it also can provoke real epileptic seizures. Low oxygen, which can result from lung disease, choking or high altitude, either can cause symptoms that imitate a seizure or provoke a real one. Another reason for loss of consciousness is a condition called transient ischemic attack or TIA. In a TIA, blood flow to piece of the brain is interrupted briefly, causing brain tissue to temporarily stop working. Some parts of the brain, such as the brain stem, are critical for the maintenance of consciousness. When a TIA affects this area, consciousness may suddenly be lost. Because loss of consciousness can be caused by several different conditions, many people who are having seizures mistakenly think they are experiencing something else.

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On the other side of the coin, are people who think they have seizures, but actually have one of the imitators. In the end, if seizures do not respond to the usual treatments, then the diagnosis should be reconsidered.

15. CONFUSION IMITATORS OF SEIZURES

Sudden confusion is a common symptom of certain types of seizures, but it also is a symptom that can be caused by one of the many seizure imitators. One common condition that can produce sudden confusion that may look like a seizure is a transient ischemic attack or TIA. TIAs occur when blood flow to the brain is interrupted briefly, causing the brain to temporarily stop working. This can cause a variety of different responses, depending upon what part of the brain is deprived of blood. A TIA affecting the speech, memory or sensory-motor centers of the brain can produce confusion, tingling, weakness or other symptoms that imitate a seizure. Another common confusion imitator, as most of us know from our own experience, is uncontrollable sleepiness. Some people who are asleep on their feet at inappropriate times may be thought to be experiencing a partial seizures. These people may be excessively sleepy because of missed or interrupted sleep, medication side effects or a sleep disorder. Two common sleep disorders are sleep apnea, in which breathing stops and starts during sleep, and narcolepsy, a neurological disorder involving sleepwake cycles. People with narcolepsy can experience cataplexy, which is a sudden loss of muscle tone and falling at a point of high emotion. This is commonly called getting "weak in the knees." But whether it stems from narcolepsy or other causes, sleep confusion usually results in an irresistible sleepiness before the attack, as well as the ability to be woken up during the attack. These factors allow doctors to distinguish a sleep problem from a seizure. During the night, some people sleepwalk, act out their dreams or have screaming attacks called night terrors. These episodes can raise a question of seizures once again. Since some seizures do occur primarily during sleep, a medical evaluation may be needed.

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In the early stages of a migraine headache, some patients may experience an aura which involves seeing shapes, colored lights and may include lightheadedness or dizziness. People who are experiencing an aura may find it hard to think straight. A migraine aura is confusing, and particularly in cases where the other symptoms of headaches are not prominent, can be misdiagnosed as seizures. Another seizure imitator that is fairly common is called transient global amnesia or TGA. During a TGA attack, a person suddenly loses the ability to form new memories and often asks the same questions over and over. A TGA usually lasts just a few hours. While TGAs are frightening, they are probably harmless and do not require treatment, just the correct diagnosis. One final condition that causes seizure like confusion is delirium or encephalopathy. Delirium is prolonged confusion that waxes and wanes. Hundreds of medical conditions, including common ones like infection or fever, can produce delirium. When delirium comes and goes a legitimate question arises as to whether the person experiencing it is having repeated small seizures. A careful neurological evaluation, including an EEG of brain waves, may settle the question.

16. MOVEMENT IMITATORS OF SEIZURES

Conditions that imitate seizures can be grouped according to which aspect of seizure they mimic. One category of seizure imitators causes abnormal movements. Many epileptic seizures involve abnormal movements, such as twisting or twitching. But other movement disorders, including conditions such as tremors, Parkinson's disease, dystonia, chorea and tics, also involve odd postures and movements. People who have these movement disorders do not show the concurrent EEG brainwave changes characteristic of an epileptic seizure, which can help to distinguish these conditions from an actual epileptic seizure. Let's look at how each movement disorder typically manifests itself. A tremor is rhythmical shaking of one body part. It looks like this. If a tremor comes and goes, it may be misdiagnosed as a partial seizure with motor manifestations. Dystonia is the continued maintenance of an abnormal posture, such as this. Dystonia can be

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confusing to a diagnostician because some seizures include dystonia as a symptom. Then again, dystonia can also be a movement disorder on its own, completely unrelated to epilepsy. Another movement disorder, chorea, comes from the Greek word for "dance." It manifests itself as if the hands are doing a little dance or fidget. A person with chorea looks extra fidgety and may try to cover up a chorea movement with seemingly normal activity like brushing their hair. Athetosis is a movement disorder that also comes from the Greek, meeting "swimming," and a person with athetosis makes arms or legs movements like he or she is swimming. Now chorea and athetosis can be combined into a condition called choreoathetosis. Another seizure movement imitator, hemiballismus, is a rare condition that shows up as violent flinging movements usually restricted to one side of the body. Finally, tics, which are habitual quick abnormal movements, can mimic seizures. Tics seem to relieve tension and are semi-voluntary, meaning that people can inhibit them, at least for a while, with effort. These movement disorders can all present in a manner that imitates the symptoms of a seizure. But remember that not everything that shakes is a seizure. If you or someone close to you has seizures or a look-alike, please seek medical attention to get the correct diagnosis and treatment.

17. PSYCHOLOGICAL IMITATORS OF SEIZURES

While many medical conditions can be confused for epilepsy, the most difficult to differentiate are those that mimic the psychological aspects of a seizure. Some conditions affect the mind in a way that produces symptoms similar to seizures and can provide real diagnostic difficulties for doctors. One such

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psychological imitator, called the breath-holding spell. A breath-holding spell occurs when a child becomes angry or startled and on an involuntary basis has a cessation of respiration. There is a pale form and a blue form. The pulse also may slow down or even pause. This can be followed by jerking. The symptoms are similar to certain kinds of seizures. A night terror is another common condition that mimics epilepsy. It is seen most often among children aged 2 to 6. During the night terror, children will let out blood-curdling screens during sleep. The children rarely remember the episodes, but the parents do. While the breath-holding spells and night terrors can be frightening, they are generally benign, and not epilepsy. On occasion, panic and anxiety can lead to episodes that mimic seizures. With anxiety can come hyperventilating, which is essentially breathing fast at a rate in excess of what the body needs. Excessive breathing may lead to low levels of carbon dioxide in the blood. This causes dizziness, numbness and confusion and may appear similar to symptoms of seizures. Hyperventilating may be the result of pain, anxiety or a panic attack.

A panic attack is a very abrupt period of intense anxiety and physiological arousal, including rapid heart rate, dizziness and nausea. There can sometimes be a sense of impending doom. Once diagnosed, panic attacks can generally be controlled with a combination of medication and psychological care. One especially confusing psychological imitator of epilepsy is called a psychogenic nonepileptic seizure or PNES. A PNES is a seizure-like event that is caused by psychological factors. Generally, the person experiencing a PNES is not aware of these factors and cannot control them. PNES's do not come from electrical discharges of the brain, as do epileptic seizures. PNES's can be diagnosed and treated. For more information on PNES's, please check out the other videos in this series.

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18. UNDERSTANDING PSYCHOGENIC NONEPILEPTIC SEIZURES

Certain psychological conditions can cause psychogenic nonepileptic seizures, which are episodes that imitate seizures. A PNES is a seizure-like event that is produced, not by abnormal electrical charges in the brain, but by psychological factors of which the patient is not fully aware and cannot control. Psychogenic nonepileptic seizures go by many names, including pseudoseizures, psychological seizures, psychosomatic seizures, psychogenic seizures. Because thoughts and feelings have impact upon our physical being, unresolved stressors often manifest as physical symptoms, be they headaches, ulcers, skin rashes or shaking and blackouts that look like seizures. Sometimes the stressors that lead to a PNES involve extreme pressure to succeed in an area of one's life. Other times, stressors are consequences of mental, physical or sexual abuse. These traumas can remain from years past, even dating back to childhood. The unconscious brain does not treat time in the same way that the conscious brain does, and old psychological issues can live on. They are even more potent if something happens today to bring back the feelings of yesterday. Therefore, a psychogenic nonepileptic seizure may result from result from unresolved stress and psychological tension dating back years. It's important to note that people with epileptic seizures list stress as one of the most common provoking factors. This means that having an event that is provoked by stress does not necessarily mean that the person is having a PNES. Family and friends of people with psychogenic nonepileptic seizures should realize that the person having the problem is not "faking," it on intentionally, but that it is an involuntary medical condition. People with PNES are a very mixed group. Some have mental disorders such as depression, adjustment disorders, personality disorders or rarely even psychotic disorders. Then again, other people with PNES have no obvious underlying mental problems whatsoever. That's why everybody needs to be evaluated and treated individually. During the psychogenic nonepileptic event, the brain's electrical activity, which is shown by its EEG pattern, remains normal. This point can be confusing even to doctors, because an EEG occasionally can be normal during epileptic seizures as well. Also, remember that the EEG is often normal between seizures in people who do have epilepsy.

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On occasion, a person can have both nonepileptic and epileptic seizures, making diagnosis even more difficult. To those who have them or see them in a loved one, nonepileptic seizures are as real as are epileptic seizures. Any seizure-like event requires appropriate diagnosis and medical care.

19. TREATING PSYCHOGENIC NONEPILEPTIC SEIZURES

Certain psychological conditions can cause psychogenic nonepileptic seizures, which are episodes that imitate seizures. Psychogenic nonepileptic seizures or PNESs are complicated because, while they look like seizures, PNESs do not result from abnormal electrical discharges in the brain. Instead, they are dictated by psychological events, which a patient cannot control. Effectively diagnosing PNESs begins with the physician considering the possibility that a persons seizure-like events may not be epileptic seizures. By listening to a careful description of the events or looking at a home video of the episode, an experienced doctor can tell whether the attack has the characteristics of an epileptic seizure. But even experienced epilepsy specialists can be fooled by descriptions alone. An accurate diagnosis often can be made by recording the episode with a video and an EEG in an epilepsy monitoring unit. In cases where the patient's history is unclear and the event cannot be recorded, then the diagnosis may remain uncertain.

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Once a diagnosis of PNESs is made, treatment is very specialized and ideally should involve a partnership among a psychiatrist, a neurologist and the patient's primary care physician. However, not all psychiatrists and neurologists are familiar with psychogenic nonepileptic seizures. You can find physicians who are by contacting an epilepsy center at a university medical center near you. Once a patient finds the right treatment team, the treatment must be individualized because everyone is unique. Psychotherapy can be useful to help a patient explore, understand and manage the stressors that led to PNESs. Patients also can train themselves to use relaxation exercises and mental imagery of a pleasant relaxing scene at the start of their events, in order to make them less intense. Treating PNESs is often compensated, because many patients with the condition are given heavy doses of antiepileptic medications. In the absence of epileptic seizures, these medications just produce side effects and make life even more difficult. Of course, remember that you should never stop taking a medication on your own. Work with your physician, because sudden withdrawal can be dangerous. If someone in your family experiences PNESs, try to keep calm, be quietly reassuring, and remember that a psychogenic nonepileptic seizure does not harm the brain. If there is thrashing or physical activity, you should protect from injury, but if your presence seems to prolong the attack it may be best to leave the person alone. In the long-term, you can help by encouraging participation in psychiatric care and their relaxation exercises. A person having ongoing PNES is generally not safe to drive. After the episodes are controlled this can change, although caution is needed. The good news is that over half the people who experience psychogenic nonepileptic seizures can become episode-free. However, this prognosis depends upon the patient's motivation, how severe the

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underlying psychological or physical disorders are, and whether good medical help can be obtained. If you or someone close to you is having either epileptic or psychogenic nonepileptic seizures, please contact a physician.

F. Treating Epilepsy 20. APPROACHES TO SEIZURE MEDICATION

Medications are the main treatment for epilepsy and there are over 20 choices. These medicines are called anti-epileptic drugs, or AEDs, but this actually is a misnomer because these medications do not prevent or cure epilepsy. Instead, AEDs work to suppress seizures. There are five principles of AED therapy that many doctors follow.

When a patient has seizures, the first consideration is whether to treat them with AED therapy. Certain types of seizures, such as simple partial seizures with only minor sensory, motor or mental manifestations, may not require treatment. Also, a first seizure may not require treatment if tests show no factors likely to produce subsequent seizures. The next step is to choose the best medication for particular patients seizures. There are no hard and fast rules for selecting seizure medications, because most work for several

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different types of seizures. Many factors are considered, including side effects, risks of a serious reaction, convenience of administration, and cost. After a medication is selected, a doctor will then decide the best AED regimen, which generally requires usage on a simple schedule. A regimen of one drug, called monotherapy, is less likely to produce side effects and drug interactions than is using multiple AEDs. Moreover, studies show that using additional drugs rarely eliminates seizures when using one drug does not. Although more than one drug is sometimes necessary, a simple dosing schedule is most likely to be followed correctly. It's important to take AEDs on a reliable schedule, because skipping medicine can result in a seizure. Side effects are another consideration. Every medication, even aspirin, has potential side effects. Seizure medicines have many because they act on both body and brain. Most seizure medicines make brain cells fire less rapidly. This is useful to control a seizure where brain cells fire at exceptionally high rates. But brain cells also fire quickly during some normal activities, such as maintaining balance, focusing eyes and thinking. All of these activities are slower and less precise with seizure medicines in the brain, which is why significant effort is devoted to balancing seizures and side effects. All too often patients experience both seizures and side effects. When this occurs, a different strategy is needed, like a different medicine, fewer medications or nonmedication therapies. Switching medications can be difficult. A doctor can help keep the process on track by providing a written dose-initiation schedule. Patients should expect a temporary period of increased side effects and possible withdrawal seizures during any medication change. Finally, AED therapy is not always forever. Tapering AEDs can be considered when a person has been seizure-free for at least two years. However, AED therapy can only be stopped once it has been established that a person has no major ongoing predisposition to seizures and has no seizure activity on a routine EEG. The person should also not have experienced problems with prior attempts to stop medications. Even if seizures have not occurred for years, medications usually are continued if an underlying problem in the brain is present, like a stroke, tumor, abnormal blood vessel or birth defect. If a person meets the conditions for tapering, there is a two in three chance of being able to withdraw AEDs successfully. The flip side is that there is a one in three chance of having a seizure after withdrawing medicine, a risk that some find unacceptably high. Also, many doctors advise not driving while withdrawing AEDs, which prevents some patients from even trying. In all cases, except emergencies, medications are tapered slowly and under care of a doctor. The goal of medication therapy is not only seizure control, but also improvement in quality of life. If side effects, inconvenience or cost make the treatment worse than the disease, do not hesitate to explore other options with your medical team.

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21. WHO GETS EPILEPSY SURGERY?

Surgical therapy to treat seizures was developed in the 1800s. Yet, while epilepsy surgery has come along way since then, it's still not for everyone. Several types of surgery can help to eliminate or reduce seizures in people with epilepsy. Brain surgery is an important decision and is usually undertaken when multiple medication trials have failed to control seizures. The vast majority of people who are treated with epilepsy surgery have partial seizures. Surgery can be performed on children, as well as infants under one year of age. Several factors are important in considering someone for possible epilepsy surgery. They are: whether the patient has seizures that are not controlled by systematic medication trials, localized seizure onset in the brain, a level of health that makes brain surgery relatively safe, and an understanding and acceptance of the risks. Generally, epilepsy surgery is considered for people who have seizures that cannot be controlled by anti-epilepsy drugs because of ongoing seizures, unacceptable side effects or both. Poorly controlled seizures or refractory epilepsy occurs in one out of every three

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people with epilepsy. For epilepsy surgery to be considered, seizures also need to be severe or frequent enough to impair quality of life, a standard that varies tremendously for different people. For some people, seizures that prevent them from being able to drive or high doses of medications that cause continual side effects, is reason enough to pursue possible surgery. Other people have daily seizures and side effects, but still do not want to consider brain surgery. Most doctors will not perform surgery until a patient has had uncontrolled seizures for at least two years, although when seizures are frequent or severe it may be considered sooner. Typically, surgery is considered only if the patient's seizures are unable to be controlled with at least two single drugs and one two-drug combination. It is critical that these medication trials are done systematically. Just one week on a drug is long enough to determine a bad medication side effect, like a rash, but it is not an adequate trial of how well the medication works. A doctor gradually increases medication doses to the maximum tolerated level to see if greater doses will effectively control seizures. Once a patient is considered for surgery, tests are performed to identify what area of the brain is giving rise to seizures. This is because some areas of the brain can be removed without changing intellect or personality. But removal of other brain areas can cause problems with language, memory, sensation, strength or other functions. In some cases, the risks of surgery outweigh the benefits, while in others the chances for seizure control are good with limited risk to vital brain functions. The decision to have surgery involves careful individualized consideration by both patient and doctor. Remember, epilepsy surgery is elective and should ultimately be the patient's decision. If you think you may be a candidate for surgical therapy for epilepsy, talk to your physician about a referral to an epilepsy center.

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22. YOUR PRE-SURGICAL ASSESSMENT, PART 1

Epilepsy surgery is not for everyone. So how is a patient considered and assessed for a surgical procedure? Before a person can even be considered for surgery, his or her seizures must persist despite medications and must also interfere with the patient's quality of life. In addition, the surgical candidate must be healthy enough for a brain operation and be willing to accept the risks of surgery. If these criteria are met, a presurgical evaluation is conducted to try and find the area where the seizures start, called the seizure focus. The best candidates are those in whom a single relatively small seizure focus is found in a part of the brain that can be safely removed.

The first part of presurgical assessment is a careful description of seizures by the patient and family. This can give clues about location in the brain where seizures arise. Next, an EEG or electroencephalogram is conducted to measure brain waves, in turn helping to localize abnormal electrical activity in the brain. While EEGs taken in between seizures can help, recordings during a seizure are most informative. This procedure usually is completed in a video-EEG monitoring unit where patients stay for several days or longer to record EEG and video during seizures. If three or more seizures show a consistent place of origin, surgery will most likely be successful.

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Neuroimaging with an MRI is another important test for localizing a seizure focus, because it may shows a scar or brain injury that is causing the seizures. When both the EEG seizure focus and an MRI abnormality are in the same region, confidence regarding the very best surgical target is increased. Another vital assessment is neuropsychological testing. Pencil and paper tests are given to measure the person's skill in memory, language and other thinking tasks. In most righthanded people, it's the left side of the brain that controls language and calculations, while the right side controls picture memory and spatial perception. Specific thinking problems shown during neuropsychological testing can help identify abnormal function in different brain areas.

Video EEGs, MRIs, neuropsychological tests are completed in all candidates being seriously considered for epilepsy surgery. Several other tests are done on an individualized basis. One such test, a PET scan, is an imaging test that uses a radioactive tracer to measure consumption of glucose in the brain. This is useful because a seizure focus may consume less glucose between seizures than normal areas of the brain.

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PET scans are often used when the patient's MRI does not show a clearly abnormal region giving rise to the seizures. Another tests that measures brain activity and may be used is called a magnetoencephalography or MEG test. This can provide a three-dimensional map of where epilepsy waves come from in the brain. If these tests suggest that surgery can help control seizures, the doctor may recommend additional tests that are more invasive. These additional tests allow direct stimulation of different part of the brain, which can help pinpoint the seizure focus and localize normal functions further. To learn more about these tests, and how they may be administered, please see the next video in the series.

23. YOUR PRE-SURGICAL ASSESSMENT, PART 2

Before a patient undergoes surgery to treat epilepsy, presurgical tests, which may be invasive, are vital to assess where in the brain seizures start. All surgical candidates must undergo several noninvasive tests, described in the prior video, during their presurgical assessment to find the area where the seizures start, called the seizure focus. If these tests suggest that surgery is likely to help control seizures the doctor often recommends additional tests that are more invasive and do come with some risks. A commonly used invasive test is the intracarotid hemisphere dominance or Wada test. It involves a catheterization, in which a thin plastic tube is put into an artery where the upper thigh and pelvis meet. The tube or catheter is carefully guided to the carotid artery and a quick acting anesthetic is injected. This is performed sequentially on both sides, putting the left and right sides of the brain to sleep, in turn allowing speech and memory to be tested. In most people, language is on the left side of the brain and memory is on both sides. However, if memory is impaired on one side, then it suggests that the temporal lobe on that side is not working well and may be the source of seizures. The Wada test helps a neurosurgeon plan safe boundaries for epilepsy surgery. For example, if memory is impaired in the right half of the brain but excellent on the left side, a right temporal lobectomy can likely be done without risk of harming memory. Meanwhile, because some seizures originate deep in the brain, their onset is not always seen clearly by scalp EEG recording. In these cases, electrodes are placed under the skull to help the doctor get a close-up look at the seizure focus. Two kinds of electrodes are used: subdural electrode grids or strips, which are put under the skull but on top of the brain; and depth electrodes, which go directly into brain tissue. The grid electrodes placed directly on the surface of the brain can get a close-up recording of seizures. These grid electrodes can help map the function, such as language or movement, of the underlying region of the brain. This is done by sending a small electric current through an

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electrode, which can inactivate a part of the brain for several seconds. If an activity like counting to ten, for example, is interrupted by this, then the part of the brain that was stimulated can be marked as a control area for speech. Similar analysis can be applied to movement, reading or other brain functions. Grid mapping is useful when seizures are close to a critically important region of the brain.

Subdural or depth electrodes can be used in surgical procedures intended only to diagnose a seizure focus, but they also can be used as part of a two-stage epilepsy surgery. In the latter case, the first stage involves recording the seizures and possibly mapping them and brain functions. The second stage involves removing the electrodes, followed by removal of the brain tissue from where the seizures arise.

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If the initial evaluation suggests that you might be a good surgical candidate, then discuss the risks and benefits of the recommended surgical procedure with an epilepsy team.

24. RESECTIVE SURGERY FOR THE TREATMENT OF EPILEPSY

Resective surgery is the most common form of surgical treatment for uncontrolled seizures. So what is resective surgery?

Resective surgery is a type of epilepsy operation in which the area of the brain responsible for seizures is surgically removed. The brain is comprised of four lobes, called the frontal, temporal, parietal and occipital lobes. Seizures most often arise from one or both temporal lobes. In the deep front part of the temporal lobes are located the most seizure prone structures in the brain: the hippocampus, which is Greek for seahorse, and the amygdala, which means almond. Because of this, temporal lobectomy is one of the most common and one of the most successful types of resective surgery.

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Access to the deep temporal lobe can be achieved in two ways. The conventional approach involves removing an inch and a half from the tip of the temporal lobe to provide access to those deeper areas. The second involves cutting into the outer brain and opening a window from the side. However it is accessed, the hippocampus, amygdala and surrounding brain are removed by a combination of cutting and suction, since brain tissue is soft. All bleeding is carefully controlled during surgery. The surgery does not remove a tiny piece of the brain, but rather a sizable part of one lobe. After the removal of the temporal lobe tissue is complete, the bone is replaced and secured to the skull and the scalp is then sutured. Whenever possible, the surgeon uses incisions behind the hairline for the best possible cosmetic results. Patients then move to a recovery room or intensive care unit. A few days post-surgery, though, most move to a normal room and are eating and walking.

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Postoperative nausea and headache are common, so patients receive medications for these conditions and possibly seizure medications as well intravenously for 6 to 48 hours. A hospitalization for temporal lobectomy typically lasts from 4 to 6 days for one-stage surgery and 9 to 14 days if a two-stage surgery is completed. Then, patients take it easy around the house for a week, at which point the surgical stitches or staples are removed. Vigorous activity should be avoided for a month or two, but a patient can generally return to work within 1 to 3 months. Patients often ask whether the part of the brain that is removed grows back. It does not. Immediately following surgery, the fluid that surrounds the brain fills in the empty area. Another common question is whether the surgery creates a scar that will produce seizures. Usually, it does not because the surgical scar is clean and does not irritate adjacent parts of the brain. This is like the difference between a plastic surgery scar and a scar from a bad accident. Once a patient has undergone resective surgery, most doctors will keep a patient on seizure medication for at least several years. Sometimes, the medication is necessary for life, although the dosage might be reduced. While resective surgery can be quite effective, it is not for everyone and is always a patient's personal choice. If you think you might be a good candidate for surgery, discussion your options with your doctor.

25. OTHER TYPES OF EPILEPSY SURGERY

In a resective surgery a portion of the brain is removed. When this is not possible, doctors may consider other forms of brain surgery to treat epilepsy.

While resective surgery is the most common type of epilepsy surgery, there are several others which can be useful. One such procedure is called a lesionectomy. A lesion is an abnormal structure in the brain, like an old scar. The scar may be present due to past trauma, bleeding, infection, stroke, abnormal blood vessels, a birth defect or a tumor. Seizures often originate around a lesion. So a lesionectomy removes it, as well as a rim of surrounding brain tissue believed to be involved in seizure generation.

Another type of procedure, called disconnection surgery, involves severing specific nerve pathways in the brain along which seizures spread. One disconnection surgery, which reduces atonic, tonic-clonic and tonic seizures is corpus callosotomy. During this procedure, the corpus callosum, which is the large fiber bundle in the brain that connects the two hemispheres, is cut. Often, the operation involves severing just the front twothirds of this area. Following this partial procedure, seizure reduction hovers around 75%.

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Later, a second operation may be performed to disconnect the remaining third of the corpus callosum, and this can improve seizure control to up to 85%. The most dramatic surgery performed to treat epilepsy is hemispherectomy. This operation involves removing and/or disconnecting one cerebral hemisphere from the rest of the brain. Hemispherectomy usually is only considered in patients with severe seizures who also have some weakness and sensory loss on the side of the body opposite from where the surgery is planned. This is because the surgery itself will cause severe weakness and sensory loss, even if it is not there already.

Another rare form of epilepsy surgery is multiple subpial transactions. This procedure is used to control seizures that stem from areas of the brain that cannot be safely removed. For example, if seizures originate in an area that is critical for language, removing this area might devastate the understanding of language or speech. A subpial transaction involves making multiple superficial cuts into the more shallow layers of the brain. These cuts or transactions interrupt fibers that connect neighboring parts of the brain and in turn disrupt the spread of seizure activity. This procedure is not as effective as removal or disconnection surgery. And only a minority of patients become entirely seizure free after this procedure. Still, major complications of subpial transactions are rare and the benefits can outweigh potential complications. No matter the form of epilepsy surgery considered, however, surgery is not for everyone and is always the patient's choice. If your seizures are not being controlled, discuss the possibility of epilepsy surgery with your medical team.

26. RISKS AND BENEFITS OF SURGERY, PART 1

Surgical treatment for epilepsy is major brain surgery. As such, it is not a decision to undertake lightly, but one to be carefully considered. Before an elective surgery, a patient and doctor must compare the risks and benefits of the operation itself to those of the ongoing seizures. While surgery has risks, seizures and high doses of medications have risks as well. Epilepsy surgery is a time and money commitment. Although surgery is usually covered by health insurance, the cost is still high, from 40,000 to over $100,000. Misperceptions and misunderstandings about surgery are common. While it is vital to have an accurate picture of potential complications, it is also important to eradicate unfounded fears. Similarly, it is critical to have realistic expectations. Many patients worry that removing a portion of their brain will change their personalities or who they are, but this is very rarely the case. For most people with uncontrolled

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epilepsy, the area of the brain that causes seizures is not functioning properly anyway. Since it is not doing what it should be doing, removing it is usually safe. Furthermore, electrical activity arising in the brain's seizure focus often impairs the functioning of other brain areas. The medical team needs to help the patient and their family understand the risks and benefits of epilepsy surgery in the context of the risk of uncontrolled seizures and high doses of medications. For example, in people with severe and frequent seizures epilepsy may be progressive and debilitating, with memory and mood problems that worsen over time. Plus, very high doses of medications can adversely affect health. Together, seizures and medication side effects can impair quality of life, including the ability to drive, work and learn. Of course, the worst complication after any epilepsy surgery is death, which occurs in less than 1 out of 1000 cases. But remember, uncontrolled epilepsy can also be deadly. Among people whose seizures are severe enough to be surgical candidates, up to 9% run the risk of dying from sudden unexplained death in epilepsy or SUDEP in a 10 year period.

What are the benefits of epilepsy surgery? Depending on the type of surgery, more than 60% of patients can become seizure free and 90% can enjoy a significant reduction in their seizure activity. Many patients report that in addition to experiencing fewer seizures, they have an improved quality of life due to reduced depression and reduced medication burden. These general considerations apply to anyone thinking about epilepsy surgery, but each type of surgery has its own risks, benefits and success rates that vary by the individual case. To learn more about specific surgeries, please watch the next video in this series.

27. RISKS AND BENEFITS OF SURGERY, PART 2

Each year, more than 2000 people get surgery to control or reduce their epileptic seizures. Some of these surgeries are riskier than others. While there are differences between the types of epilepsy surgery which are performed, many of the same considerations apply to all of them. When a doctor presents epilepsy surgery as an option, it is important that he or she places the risks and benefits of the procedure in the context of the risks of uncontrolled seizures or high doses of antiepilepsy medications. There are many types of surgery, and each is associated with different risks and benefits.

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The most common type of epilepsy surgery is called a temporal lobectomy. This is the removal of part of one of the temporal lobes of the brain, areas associated with memory and emotion. Following a temporal lobectomy, there may be a slight decline in memory and word finding, especially for rarely used words. These potential problems are most likely to occur if the operation is performed on the left temporal lobe, which controls language functions. After a temporal lobectomy, the most common emotional changes are improvements in anxiety and depression. However, anxiety and depression can occasionally develop for the first time after a lobectomy. If it does, it is usually temporary and responds well to medication. Although some patients experience a minor loss of vision on the outer part of the side opposite from the surgery, it is usually so slight that most are unaware of it. The most serious risks of temporal lobectomy are a 1 to 2% chance of stroke and a 0.1% risk of death. However, because epilepsy surgery is elective and allows for preparation, the risks are reduced to the lowest possible levels in neurosurgery. After a temporal lobectomy 55 to 75% of patients are free of seizures that impair consciousness. An additional 10 to 30% have occasional seizures, but enjoy a significant reduction in seizure activity. Unfortunately, occasional seizures that impair consciousness will still restrict driving and certain other activities. However, up to 15% of patients notice no improvement post-surgery. Most people who become seizure free after surgery still require anti-epilepsy medications, but often that lower doses than before. Some patients can eventually come off all medications, but this is not the primary goal. Freedom from seizures and medication side effects is considered success. A lesionectomy is another type of epilepsy surgery. Lesionectomy and other epilepsy surgeries that remove brain tissue generally come with a risk of stroke that is just 1 to 2%. Depending upon the specific location of the seizure focus, there may be other risks to vital function, including language, movement or sensation.

Corpus callosotomy, another form of surgery, carries a slightly higher risk of stroke or problems with attention or behavior. The corpus callosum is the largest group of fibers or wires that connect the left and right sides of the brain. After partial corpus callosotomy, which severs the front two-thirds of this fiber bundle, seizure reduction is around 60 to 80% for certain seizure types, including tonic-clonic, atonic and tonic seizures. After the complete procedure, which often involves two separate surgeries, reductions rise to 80 to 90%. Another surgery, called hemispherectomy, is the removal and/or disconnection of half the brain. Although the functions of this half of the brain are often seriously impaired before surgery, any remaining functions are lost after the procedure. However, hemispherectomy does provide almost complete seizure relief in 75% of patients.

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When deciding if epilepsy surgery is right for you it can often be helpful to obtain the opinion of experts at another epilepsy center or to speak to patients who have had surgery before. Bottom line: if someone is a good candidate for surgery and epilepsy significantly impairs quality of life, surgery is worth seriously considering.

G.

Living with Epilepsy

28. SAFE DRIVING FOR PEOPLE WITH EPILEPSY

Driving is not just a convenience. This privilege may also represent freedom, independence and economic self-sufficiency. Are these benefits off-limits for people with epilepsy?

Many people with epilepsy are able to drive, but before you take the wheel, let's look at a few statistics. Between 5 and 10% of Americans crash a car each year. For people with epilepsy, the rate is about 30 to 50% higher. While that sounds alarming, a 50% risk increase is far below the higher crash risk for drinking drivers, young male drivers or elderly drivers. Not every car crash involving a person with epilepsy is from a seizure. Sometimes, the crash results from normal causes. Other times, sleepiness and delayed reactions, which can stem from seizure medications, might lead to a crash as well. Of course, if someone is having frequent seizures with loss of awareness, its not wise for them to be driving. So how long should a person be seizure-free, known as the seizurefree interval, before seizures are sufficiently controlled for safe driving? Different states in the US have different answers to this question, varying from three months to two years. Others leave it to the discretion of your physician.

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Most states do make exceptions for people with certain types of seizures, including seizures too minor to affect driving ability, seizures with a prolonged and consistent aura or warning sign, and seizures that occur only in an established pattern during sleep. So how does the state find out if a person has seizures? Most patients and epilepsy doctors believe that reporting of seizures should be the responsibility of the individual who has them. However, six states in the US: California, Nevada, Oregon, Pennsylvania, New Jersey and Delaware, currently mandate that physicians report loss of consciousness and seizure disorders. Unfortunately, required reporting can be harmful to the patientphysician relationship and it may encourage concealment of seizures. For this reason, attempts are underway to change these mandatory physician reporting requirements.

Commercial driving uses a stricter standard. In the US, these rules require federally certified drivers to be seizure-free for at least ten years and off seizure medications. Interestingly, some people such as cab drivers or Highway Patrol do not require a commercial license, but spent much of the day driving anyway. Some doctors, including me, believe that these people should be seizure-free for longer periods than the average driver. In closing, if you experience seizures, here are some things to consider before you get behind the wheel. Do not drive until you and your medical team have determined that it is safe to do so, and notify your physician if your seizure condition has deteriorated. Be aware of your state and national laws about seizures and driving. And should you feel a seizure coming on while driving, it's best to stop in the road and remain in the car. Pull over only if you are sure you can make it safely.

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If you or someone you know has seizures, remember to put safety first, both the publics and your own.

29. EPILEPSY AND EMPLOYMENT

Most people with epilepsy can work productively at full time jobs, yet people with epilepsy have about twice the unemployment rate of the general population. Why is that? Often, people with epilepsy want to work but may encounter employers afraid of the potential effects of a seizure on the job. These employers may worry about liability, missed work or customer seeing someone having a seizure. What these things can happen, they are not valid reasons to avoid hiring people with epilepsy. The only time when a potential employee's epilepsy is relevant to the hiring decision is in a case where seizures on the job would endanger the persons or the public's well-being. Such exceptions might apply, for example, to pilots, bus drivers, firemen, roofers and tree cutters. In addition, people with seizures should avoid work that involves driving, working underwater or in other dangerous locations, or spending prolonged periods around fire, dangerous machinery or chemicals. Despite these limitations, over 90% of jobs can be done and done well by people with epilepsy. Just as importantly, it is illegal to discriminate against people with epilepsy. This became law when President Bush Senior signed the Americans with Disabilities Act or ADA of 1990, which listed epilepsy as a protected disability. The bill was championed by Tony Coelho, who was then the Democratic whip in Congress. Coelho, who is publicly a person with epilepsy, is the honorary lifetime Chair of the Epilepsy Foundation of America, the primary organization in the US advocating for people with epilepsy. The ADA applies to government employers or contractors, educational institutions and private businesses with over 15 employees. Knowing this, should you disclose your epilepsy on a job application? Generally, the answer is still no. It is not legal for an employer to ask about disabilities, medical conditions or what medications you are taking. Employers are, however, are allowed to ask whether you have any conditions that would prevent you from fulfilling the duties of the job, and if you do, you should answer honestly. Once you have a job, you will have to decide whether to let your coworkers, supervisor or human resources department know about your seizures. So what if you do have a seizure on the job and it causes a problem? Once again, the ADA comes to your aid, stating that the company must attempt to make reasonable accommodations for you. For example, there might be another position in the company that would be less problematic, or you might be excused from overtime if missing sleep provokes seizures. If you have been unfairly treated on the job because of epilepsy, you have at least three levels of recourse. First, you can attempt to work the problem out within the company.

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Second, you can contact your regional Equal Employment Opportunity Commission, which you can find by visiting their website at www.eeoc.gov. The EEOC will hear your story and decide whether to pursue it on your behalf at no charge. If they take your case, they may communicate with your employer or pursue legal action. The third option is to hire an employment discrimination attorney. While this may be successful, it also can be expensive. No matter the job, people with epilepsy must want to work and be able to perform the job to gain employment, just like people do not have seizures. Simply put, if you have epilepsy and want to work, you have options, opportunities and legal rights. Look into them.

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30. EPILEPSY AND SAFETY

If you have epilepsy, it's important that you be aware of a few simple ways to protect your safety. People with epilepsy know that seizures can provoke injuries. While it's important to be smart, and use common sense to avoid potential injuries, the goal is to live life as fully as possible.

People with frequent seizures should exhibit special care in water, including bathtubs. It may be safest to shower using a hand shower while sitting on a stool. When swimming, people with epilepsy should always be accompanied by an informed companion.

Special caution is needed around cutting and chopping machinery or in other potentially dangerous situations such as heights. People with seizures should also be careful about burns near the stove or fires. Cook on the back burner to reduce spill or burn risk, should a seizure occur.

In very rare instances, seizures can cause fatalities, either from injuries or from the poorly understood condition called SUDEP, an abbreviation for sudden unexplained death in epilepsy. Consult a medical team to discuss precautions to avoid this (some cases of SUDEP cannot be prevented). Aside from the risk of injury from a seizure, be aware that all medications, including antiepilepsy drugs, have potential risks. For example, over years certain seizure medications can weaken bones. Of course, the risks of medications must be balanced against the risk of seizures and the limits that they put on lifestyle. In early 2008, the FDA reported four suicides in about 28,000 patients taking epilepsy medicines, versus none in patients taking a placebo or sugar pill. Other patients reported having suicidal thoughts. Although these results are significant, for most people this FDA warning is just something to know, not a reason to change medicines. However, if you have symptoms of depression or thoughts of suicide, discuss them with your doctor immediately. Many epilepsy medications have interactions with other drugs, and can change the side effects of other medications. Some anti-epilepsy medications reduce the effectiveness of

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low dose birth control pills, by causing the liver to clear the hormones were quickly from a woman's body. Unexpected pregnancy can result. If you are on antiepileptic medication and might get pregnant, talk to your medical team about taking folic acid to reduce the risk of birth defects. Some groups are genetically inclined to certain side effects. For example, people of Asian descent may be predisposed to get a dangerous rash when starting carbamazepine. People with epilepsy should discuss potential adverse reactions or drug interactions with their medical team.

Many parents who have a small child and epilepsy worry about dropping or otherwise harming the child during a seizure. This is a very rare occurrence, but some precautions can be taken. Carry the baby as little as possible or use a pouch. Change the child on a floor rather than a raised table. Also, don't leave the baby in water and get help to supervise the baby in dangerous situations. With tonic-clonic seizures, ensure that they do not bang into objects or the ground during the episode. Turn the person on their side so that secretions are not inhaled. Contrary to common belief, do not put anything in the mouth since bites, broken teeth or inhalation of the object can result. If the seizure continues for more than five minutes, not counting wake-up time, or rapidly goes into another seizure, then call 911 immediately. This advice may be helpful, but it does not replace individualized medical counsel, which you should obtain from your health care team.

31. RECREATION SAFETY FOR PEOPLE WITH EPILEPSY

Having epilepsy does impose some restrictions on certain recreational activities. All too often, families or medical advisers of people with epilepsy place a heavy blanket of restrictions over all activities that may even remotely lead to an injury. While reasonable precautions, like not allowing someone with uncontrolled seizures to fly a plane, are sensible, excessive restrictions can take the fun out of life and further stigmatized a person with epilepsy. So how do we decide which activities are reasonable and which are not worth the risk? There is no general answer to this question, however, four points should be considered.

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The first point to look at is the nature of the persons seizures. Some seizures are minor and do not pose much risk. They may be the simple partial type, which occur with only an internal feeling or a fleeting sensation. Complex partial seizures and absence seizures are more of a risk during recreation, because of the associated confusion and memory loss. Tonic-clonic seizures, meanwhile, present an even higher level of risk for injury. Second, it is important to look at how well a persons seizures are controlled. While there is no precise definition of seizure control, patients who have not have seizures for a year or several years are considered to be in good control. Meanwhile, those having several seizures per month have poor seizure control. The boundaries are imprecise, because even after years of being seizure-free another seizure is always possible. Third, the risk level of an activity should be considered since different recreational activities pose different risks. People with seizures usually can participate in low-risk activities, even if their seizures are not in good control. But a medical care professional first should be consulted Some low risk activities are running, bowling, golf, baseball, basketball, soccer and volleyball. Medium-risk activities may be done if seizures are mild or infrequent, but of course review your individual circumstances with your medical team. Some medium-risk activities include football, hockey and ice skating, bike racing, gymnastics, horseback riding, swimming in shallow water with a buddy, and boating. As a general rule, if having a seizure during a recreational activity would likely cause you significant harm, then use common sense and avoid the activity.

High-risk recreational activities include hanging gliding, motor sports, skiing, competitive skateboarding, mountain or rock climbing and scuba diving. Some doctors recommend not engaging in high-risk recreational activities at all if you have a history of epilepsy, but at the very least, a person should not participate in high-risk recreation unless he or she has been seizure-free for years.

A final consideration in determining what recreational activities are safe for a person with seizures is the risk level that person is willing to assume. Doctors and families can and should give advice, but assuming that the person with epilepsy is mentally competent, he or she should make the final decision.

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EEG for Beginners

Robert S. Fisher, M.D., Ph.D., Steve Cordova, REEG/EPT/CNIM Indications for an EEG Since the days of Richard Caton in 1875, it has been known that the brain generates electricity. In 1929, Hans Berger, with a one channel tracing, showed that the electricity of the human brain could be recorded, and that it changed with processes such as eye opening and closing and active thinking. The recorded rhythm, first called the Berger rhythm and then the alpha rhythm, is an 8-12 per second posteriorly maximal rhythm that occurs when the subject is in a restful (but not asleep) state. In the 1930's multichannel EEG recordings came into play. Gibbs and associates described (after Berger) patterns in the EEG associated with epilepsy, including spikes and waves (see below for examples). Grey Walter and others showed focal changes such as high amplitude slow waves that could occur over a variety of cerebral lesions. From the 1930's to the 1970's, the EEG served as the noninvasive study to assist with localization of cerebral dysfunction. It was always used, by those most expert in its interpretation, as an adjunct to the history and neurological examination. The EEG co-existed with angiography and pneumoencephalography, two invasive tests. With arrival of the CT scan, and later the MRI, the EEG lost its primacy as a test to localize structural abnormalities. EEG still has several important indications. The main ones are listed in Table 1. Table 1: Indications for EEG - Assistance with diagnosis and classification of seizure disorders - Confirmation of encephalopathy by diffuse slowing of EEG rhythms - Localization of functional lesions when imaging studies are negative - Diagnosis of sleep disorders - Confirmation of brain death - Prediction of prognosis in coma - Identification of a few "signature" disorders (see below) Herpes simplex encephalitis (PLEDS) Jakob Disease (periodic frontal waves) Hepatic encephalopathy (triphasics) The EEG is perhaps most useful in diagnosis and classification of seizure disorders. A section below reviews the EEG findings in epilepsy. EEGs can be focally abnormal even in the absence of visible change on an MRI. An example might be the EEG of a TIA or a small stroke before edema leads to evident change with neuroimaging. The EEG reflects ongoing electrical activity, and this activity becomes immediately abnormal when the brain receives an insult. Sleep disorders include narcolepsy, sleep apnea, various parasomnias, and several other conditions. Narcolepsy can be diagnosed by a combination of clinical history and an EEG showing rapid descent into REM sleep. EEG is good for staging sleep on the basis of characteristic sleep potentials such as vertex waves, K complexes and spindles (see section on sleep below).

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In brain death, the EEG becomes flat. EEG is generated in cortex, and survival of brain stem reflexes may be seen with absence of cortical rhythms. This is a decorticate state rather than true brain death. Similarly, a patient may have a persistent vegetative state with a massive diffuse cortical injury, but still maintain enough neuronal activity to generate some EEG. Barbiturates or other depressant drugs can artifactually flatten an EEG. Severe hypothermia, with temperatures less than 28o C can also flatten the EEG. No EEG finding is pathognomonic of a disease, but some conditions have characteristic EEG signatures, and an EEG may be done to help rule them in or out. Hepatic encephalopathy is associated with triphasic waves (illustrated below), but other metabolic encephalopathies and nonconvulsive status epilepticus can also show triphasic waves. Periodic lateralized epileptiform discharges (PLEDs) are seen in herpes simplex encephalitis, stroke, or on the evolution of focal status, as well as a miscellaneous group of other less common findings. If herpes encephalitis is under consideration, the finding of PLEDS helps to secure the diagnosis and to lateralize a site of infection. Subacute sclerosing panencephalitis (SSPE) is a chronic measles infection in children with very high voltage bifrontal spike bursts. Jakob-Creutzfeldt disease shows periodic frontal sharp or slow potentials. In fact, these are often sought, but periodic sharp potentials are neither entirely sensitive for Jakob-Creutzfeldt disease, nor specific. Indications for an emergency EEG are few: to rule out subclinical status epilepticus, evaluate for herpes simplex encephalitis, and determination of brain death. In patients who are encephalopathic from an unknown cause, the EEG is especially helpful to rule out epileptiform activity or focality. Occasionally, a normal EEG, with reactive alpha rhythm will suggest that a comatose patient is either locked-in or having psychogenic episodes. THE MINIMUM OF THEORY EEG is a representation over time of voltage generated by electrodes recorded at different regions of the brain. The EEG is produced by synaptic activity of cortical neurons. As currents flow through the extracellular space and into and out of neurons regions of the extracellular space are left more negative or more positive than adjacent regions of brain. The extracellular space becomes relatively more negative at the site of a seizure focus. This occurs because the positive ions sodium and calcium enter excited (depolarized) neurons, leaving behind a relative local excess of negative charges. The EEG is in electrical communication with the extracellular space and detects this local negativity. Conversely, inhibitory synaptic activity causes positive ions (primarily potassium) to exit the intracellular space to the extracellular space and a negative ion (primarily chloride) to enter the cell, causing a regional EEG positivity. Voltages must always be recorded between two points: like a height, it is an energy level with respect to some other place. There is no such thing as a voltage at a given point. A ground or reference level is 228

always involved, even if it is assumed the electrical level of a ground lead in a wall plug. This requires that every channel of the EEG be a pair of voltages. In general, there are two types of EEG machine hookups: bipolar and referential. "Monopolar EEG" is a misnomer and an electrical impossibility. Bipolar montages link pairs of EEGs that are closely spaced on the head. Referential EEGs use the second input of the paired inputs as a standard lead against which to compare all the others. This for example could be a lead attached to the ear, or to the vertex of the head in a central location. In general, bipolar recordings give cleaner signals, but miss electrical events that are common to both electrodes, since they are subtracted out in the differential amplifier for that channel. EEG interpretation guidelines therefore suggest that recordings use both bipolar and referential connections during a study. The specific order of electrode pairs is called a montage. Different montages are used in different EEG labs, and several montages are used typically in each study. Why? Historically, this was because the number of amplifier channels in the old EEG machines did not permit coverage of the entire head in one montage. This is no longer a problem, but electroencephalographers have gotten used to a slightly different appearance of potentials in different montages, and sometimes one montage will show a spike or a noteworthy potential that is electrically cancelled out in another set of electrode pairings. Because it is a bother for the novice to keep track of which electrodes are where, for teaching purposes only, the longitudinal montage is used exclusively in this introductory exposition. Illustrations portray only one printed page, or 10 seconds, of EEG. A clinical EEG comprises at least 20 minutes of recording time with views in several montages. Proper interpretation requires evaluation of the entire record. The longer a time sample is perused, the more chance there is for uncovering an intermittent abnormality. Skill with full recordings can only be acquired with lengthy experience in supervised interpretation of real EEGs. Figure 1 illustrates the longitudinal montage. The beginner should copy the page for reference, when looking at EEGs. In the international 10-20 electrode naming system, electrodes are placed at 10% and 20% intervals around the head, judged by skull landmarks such as the nasion (frontal) and inion (occipital). Odd electrodes denote left-sided placements and even right-sided placements. Subscript z's indicate midline electrodes. Fp is frontopolar, F is frontal, T is temporal, C is central, P is parietal, O is occipital and A is for auricular (ear). A problem with the 10-20 system is lack of an electrode that falls directly over the anterior temporal region, which is very important for location of seizure discharges. F7 and F8, while technically frontal, are the closest electrodes to anterior temporal. EEGs are filtered to remove unwanted frequencies. Filtering cleans up the trace, but may remove spikes (high filtering) or slow waves (low filtering) of biological interest. EEG signals recorded at the scalp are on the order of 10-100 microvolts in amplitude. By comparison, EKG signals and gross muscle potentials are several millivolts, a thousand times larger. EEG signals therefore are easily overwhelmed by artifacts. Most EEG phenomena noticed by beginners are artifacts. Eye blinks are usually the most prominent artifact. Eye blink artifacts are large potentials maximal in the frontal leads, since frontal electrodes are situated close to the eyes. The retina is negative with respect to the cornea. When people blink the Bell's phenomenon causes them to look up, which moves the negative retina away from the Fp1 and Fp2 electrodes. This creates a relatively positive (downgoing) deflection in channels with Fp1 and Fp2 as the first of the pair.

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Muscle artifact is high amplitude irregular activity, usually in the frequency range of about 20-50 Hz. Electrode pops are sudden deflections in an electrode, with an exponential return to baseline. These usually result from static electricity or capacitive or inductive currents occurring in an electrode. Electrode shaking produces a dramatic pattern in channels comprising that electrode (usually two adjacent channels) of irregular up and down movements. EKG gives an important biological artifact. EKG usually is of higher amplitude on the left side of the head (Einthoven's triangle). Subtraction of adjacent channels may therefore show some residual potential attributable to the heartbeat. When EKG artifact fades in and out of the recording, it sometimes can be mistaken for spikes. A very large part of practical EEG reading consists of learning to ignore artifacts. The reader must sometimes suspend judgment on whether a potential is an artifact until later in the record when it may more clearly be revealed as a biologic potential or an artifact. FREQUENCY COMPONENTS OF THE EEG Each EEG channel represents a mix of frequencies that span a continuous range determined by the low and high filters, and by the underlying biological activity. Historically, the frequency ranges have been divided up into arbitrary discrete settings. They are named in Greek order of historical discovery and discussion, rather than low to high frequency numbers (Table 2). TABLE 2: FREQUENCY RANGES OF THE EEG 0 - 3 Hz: Delta 4 - 7 Hz: Theta 8 - 12 Hz: Alpha > 13 Hz: Beta In both a visual and mathematical sense, any EEG segment can be decomposed into component frequencies (Fig. 2).

3 Artificial sine waves of different periods

Waveform from summing the waves above

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FIGURE 2: Waveform decomposition Delta activity produces an underlying undulation of the EEG. Riding on top of delta activity may be frequencies in the other bands, such as components of alpha and high frequency "jittery" activity in the beta range. With practice, the electroencephalographer develops the ability for visual frequency analysis, i.e., detection of the underlying components of slow, medium and fast frequencies in each channel. Focal slowing or focal decreases of beta activity may reflect local underlying pathology. THE NORMAL EEG Figure 3 shows a page from normal EEG tracing. Each EEG channel is a record of voltage over time. The calibration marker shows one second and 100-microvolt standards. Table 1 framework for interpreting the normal EEG.

Table 1: Interpreting the normal EEG - Overall Amplitude - General Left / Right Symmetry - Alpha Rhythm - Beta Frequencies - Theta Frequencies - Generalized or Bilateral Delta - Epileptiform Potentials - Normal Variants - Response to Activation (Photic and HV) - Changes During Sleep - Correlates of Notable Behaviors - Summary and Comment

The order of the statements given in the table is not critical, except of course that summary and comment should come at the end. Not all categories apply to every record, and comment on a category may be omitted if not relevant to a particular study. The reader need not, for example, say that no epileptiform discharges occurred, but it may be helpful to do so if the request for study is done to rule out such activity. Normal EEG background voltages are in the range of 30-100 microvolts. Records with all non-artifactual activity less than 20 microvolts are low voltage, and records with voltages 231

more than 20, but less than 30 microvolts, are lower than average. Low voltage records can be a normal variant, but low voltage also occurs with anoxic-ischemic injury, depressant drugs, very thick skulls, bilateral scalp vein i.v. leaks, bilateral subdural hematomas, advanced alcohol abuse, Huntingtons Disease, possibly vertebrobasilar insufficiency and several other conditions. Low voltage records are never normal in babies or young children. High voltage records are worrisome in the neonatal and infantile period for the possibility of hypsarrhythmia. At any age, a high voltage record raises concern for seizure discharges. Voltage asymmetry is abnormal if it is sustained for more than a few seconds. Be cautious about technical factors, and especially the relatively flat single channel, which most often is artifactual. A voltage asymmetry does not, in itself, specify which side is abnormal. One side may be flat with loss of normal rhythms and voltages, and it will be abnormal. Alternatively, the high amplitude side may have high amplitude slowing, which makes it abnormal. Other factors such as presence of normal rhythms such as the alpha rhythm, or presence of abnormal rhythms such as focal delta activity or spikes, are used to tell which side of an asymmetrical record is abnormal. The alpha rhythm should be between 8 and 12 Hz, should wax and wane, and have a posterior maximum, i.e., parieto-occipital. Alpha can spread into any electrodes of the 10-20 system except for Fp1 and Fp2. The alpha rhythm is most prominent when the subject is quietly relaxed with the eyes closed, but not asleep. About 5% of people have no detectable scalp alpha rhythm; this is notable, but not in itself abnormal. The alpha rhythm usually is higher on the right side of the brain. Beta activity, a fast rhythm of 13 per second and greater, is visualized on the EEG as a "jitteriness" of the trace. The fast activity is fused on top of slower wave patterns. A record with decreased beta activity is seen as a record that is too smooth in its contour. A large amount of beta is not an EEG abnormality, and it usually results from medication effect. Paradoxically, barbiturates, benzodiazepines, chloral hydrate and other sedative medications increase beta. Decreased beta locally is said to be an indication of cortical dysfunction. In contrast, presence of focal slowing is said to be a sign of underlying white matter disease at the white mattercortical junction. These rules, however, vary in practice. Theta (4-7 per second) and delta (0-3 per second) frequencies are assessed in the EEG interpretation. A certain amount of theta activity in the waking state is normal, but the adult EEG should not contain any delta, except during stages of 232

so-called slow wave sleep (see below). Excessive theta or any delta is a sign of slowing of the rhythms.

Diffuse Slowing
Figure 4 shows an EEG that is significantly slowed in overall frequencies, comprising considerable theta and delta activity. An EEG can be diffusely slow in several different ways. First the alpha rhythm may be below 8 per second. Second, there can be decreased beta in the record (excessive smoothness of the traces). Third, there can be excessive 4-7 per second theta activity, which is a judgment call based on several factors such as the degree of drowsiness, the age of the patient, whether the theta is more in the 4-5 or 6-7 range, and how high the amplitude is of the theta. Fourth, there can be any delta activity in the waking record of an adult. The delta may be continuous, intermittent, impressively rhythmical (monomorphic), or irregular (polymorphic). When the slowing is in the form of frontal, intermittent and rhythmical, delta activity, it is named under the acronym FIRDA, which stands for frontal intermittent rhythmical delta activity. All of these different ways of slowing the EEG are, to our current state of knowledge, caused by the same broad list of etiologies. We do not know why slowing presents in so many different ways. Anything that would cause a metabolic encephalopathy or delirium, or dementia could cause the EEG to become diffusely slow. Examples include anoxia-ischemia, post-ictal state, diffuse meningitis, increased intracranial pressure, drug intoxication, severe hyponatremia, advanced dementia, and literally hundreds of other potential causes. Diffuse slowing on an EEG is conceptually equivalent to nonspecific ST-T wave changes on an electrocardiogram: definitely abnormal but nonspecific as to etiology. Diffuse slowing should be distinguished from focal slowing, since the latter implies an underlying focal cortical dysfunction. EEGs can be useful to psychiatrists in determining presence of organicity. Neither anxiety nor depression, nor psychosis alters the EEG patterns. Therefore, if the EEG is diffusely slow, then the subject has evidence for an underlying delirium or dementia. Unfortunately, many medications can make the EEG slow, including high doses of neuroleptics, sedatives, tricyclics, lithium, and many others. The EEG should not be called slow if the slowing only appears in the drowsy state, since this type of slowing is a normal transitional state.

Diffuse Voltage Changes

A flat EEG is said to show "electrocerebral silence". The reader must rule out technical factors before reading a record as consistent with electrocerebral silence. Amplification should be at least to a level of two microvolts per mm, compared to the standard of seven microvolts per mm, in order to call a record flat. Artifacts become prominent when the amplification is increased. These artifacts include EKG electrical artifacts, ballistocardiograms as electrodes move with heart pulsation, electrical noises, respiratory-ventilator associated movements and IV drip artifacts. A flat EEG has no cerebral activity above the range of 10 microvolts. Flat EEGs do not equate with brain death, since barbiturate overdose and hypothermia may give false positive flat EEGs that subsequently return to normal. Additionally, brainstem activity may not 233

be visible directly on an EEG. Many hospitals no longer require EEGs for the determination of brain death, if the clinical picture and cause of the illness is clear, and the neurological examination is otherwise consistent with brain death. Some EEGs are not isoelectric, but show only low voltage activity throughout the entire record, with absence of normal alpha rhythms and with no reactive changes in the EEG, as the patient is stimulated. Such a record is not "flat", but after anoxia, ischemia or head trauma, it has a grave prognosis. The EEG may demonstrate a so-called burst suppression pattern, which comes in several forms. With a burst-suppression pattern, the EEG is flat for a stretch of several seconds, and then there is a burst of electrical activity. The electrical activity may be somewhat spikey, or it may be comprised of mixed slower frequencies. Burst suppression is one step better than an almost flat record, which is one step better than a flat record. Burst suppression can also be produced by high doses of barbiturates and brain suppressant medications. Desired dosages of barbiturates can in fact be titrated to the length of the flat EEG. FOCAL SLOWING After a description of the overall voltage and symmetry and frequency spectrum in the alpha rhythm, the next thing the reader should do is detail presence of any focal abnormalities. This could be focal decrease or increase of voltages, or focal slow patterns. Figure 5 shows an example of an EEG with clear focal slowing over the left temporal region, seen in the top three channels. Focal slowing may be in the theta range or in the delta range, or it may vary throughout the record. Prior to the days of CT scanning and MRI, this was the noninvasive method to localize an underlying lesion, for example, tumor, abscess, subdural hematoma, traumatic scar, or infarct. Focal slowing on an EEG is a strong abnormality.

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INTERICTAL SPIKES AND SHARP WAVES Epilepsy is a clinical diagnosis based on a history or observation of recurrent episodes consistent with seizures. EEG can support the diagnosis of epilepsy. Table 4 lists several key statements about the role of the EEG in diagnosis of epilepsy.

Fp1F7T3-T5 T5-O1 Fp2F8T4-T6 T6-O2 Fp1F3-C3 C3-P3 P3-O1 Fp2F4-C4 C4-P4 P4-O2 100 1 sec

TABLE 4: Role of the EEG in diagnosis of epilepsy - A normal interictal EEG does not rule out epilepsy - Presence of spikes or sharp waves is not in itself diagnostic of epilepsy - The EEG is usually abnormal during a seizure - Deep frontal lobe seizures or very focal seizures are exceptions - EEG can help classify type of epilepsy - EEG can help localize site of a seizure focus - Repeat EEGs, sleep EEGs or activation procedures may bring out abnormality - The most difficult cases may require video-EEG monitoring

EEGs in patients with seizures are interictal, ictal or postictal. Interictal EEGs may or may not show spikes (discussed below), which are markers of regions of brain with epileptiform 235

potential. Spikes usually are subclinical and can even occur in a small percentage of the population without any history of seizures. Of 13,658 healthy young men examined for Air Force training in the United Kingdom, 0.5% had an unequivocally epileptiform EEG pattern. As many as 5% of healthy children in the age range of 6-12 years may have epileptiform EEG changes. Epilepsy remains a clinical diagnosis. The electroencephalographer should resist the temptation to make a diagnosis of epilepsy, since spikes can be benign. Phrases such as epileptic discharges, epileptic spikes, and seizure discharges are misleading in an EEG report, and should be used with caution. Regrettably, the more correct term, epileptiform activity, is not widely understood by clinicians. Slightly less than half of the people with seizure disorders will fail to have spikes on a single interictal 20-30 minute EEG. Repeat of the EEG up to four studies, with sleep deprivation and activation procedures can increase the yield to about 80%. Nevertheless, failure to observe spikes does not rule out a seizure disorder. Presence of spikes only confirms a seizure disorder if there is a good historical picture for seizures. During a seizure the EEG is abnormal over 95% of the time, exceptions being certain very focal seizures or seizures occurring in the depth of the brain with little projection to the surface. In the postictal state, i.e., a few seconds to up to an hour after a seizure, the EEG may be diffusely or focally slow. The overwhelming majority of seizure-like events with negative EEGs during the episodes are nonepileptic seizures (pseudoseizures). Never treat the EEG! Too many people are on inappropriate antiepileptic medication because of a funny type of spell coupled with some questionable sharp activity on an EEG. Many things that look sharp on an EEG are normal potentials or normal variants. Figure 8 shows an example of an interictal spike, located in the right temporal and central regions. Spikes are "pointy" potentials that have a certain size, shape, and usually an after-going slow potential that sets them aside from artifacts and other slower natural EEG potentials. Spike recognition is very much a visual phenomenon, although several computerized spike detectors have defined certain rules to pick spikes out of ongoing digital EEG traces. Studies presenting the same records to different electroencephalographers show a 60-90% agreement of whether something represents an individual spike. Designation of a potential as a spike is clearly a judgment call rather than an absolute finding. Some potentials look very much like spikes, for example vertex waves of sleep (see below). These potentials are distinguished from spikes by the context in which they appear. A vertex wave, for example, appears over the vertex during stage I sleep. These context-dependent decisions make EEG reading an art rather than a science. The pathophysiological correlate of an interictal spike is a collection of synchronously discharging neurons. Spikes are locally negative because positive ions, sodium and calcium, travel from the extracellular space into the neuron during depolarization and excitation of a neuron. This leaves behind a relative extracellular negativity, which is detected by the EEG. In a referential recording, spikes may be localized by determining where the amplitude is highest (technically where the amplitude is changing most rapidly with respect to the neighboring electrodes, but highest usually works in practice). In a bipolar montage, spikes are localized by phase reversal. An interictal spike is defined as being a sharp potential less than 70 msec in duration. Sharp waves have a similar significance to spikes, but are between 70 and 200 msec in duration. The literature is inconsistent as to where this duration is measured, and some measure it at baseline, others halfway up the spike. The current authors prefer the latter measure. Interictal 236

spikes are usually considered subclinical; however, careful neuropsychologic testing can demonstrate deficits during runs of interictal spikes.

Other Seizure Patterns

Different seizure types have different EEG correlates, although there is not a unique oneto-one correspondence. The next figure shows classical 3-4 per second spike wave bursts of the type seen in absence (petit mal) epilepsy. Spike-wave bursts typically last 1-10 seconds. They are called generalized, but in fact they tend to have a fronto-central maximum. Spikes can be better formed in some channels than others, and the classical morphology is usually most impressive in a referential montage because of wide field subtraction cancellation in adjacent electrodes. The electroencephalographer may observe occasional asymmetries, with potentials being a little larger or earlier on one side than the other, and a judgment has to be made as to whether there is a consistent lead-lag relationship among the channels. If there is, the potential may represent secondary bilateral synchrony, rather than primary epilepsy. Minor asymmetries are usually considered consistent with primary generalized epilepsy. There is no phase reversal in typical 3-4 per second spike waves, and the presumption that they are potentials paced from a distance (perhaps thalamus), and generated in deeper layers of cortex. Technicians may note behavioral changes, or alternatively, "no clinical signs (NCS)" during the spike-wave bursts. Behaviorally, the longer the burst, the more likely there will be an interruption of awareness. The terms "interictal" and "ictal" do not make sense for spike-wave bursts because of this continuum of behavioral interruption as the burst lengthens. 237

Spike waves can occur at frequencies other than 3-4 per second, and the frequencies are clinically significant. Slow (sometimes called "atypical") spike-waves in the frequency range of 1.5-2.5 can be seen in the Lennox-Gastaut syndrome. This is a severe epileptic disorder, with the defining triad of multiple seizure types including tonic or atonic seizures, variable degrees of mental retardation and slow spike-waves on the EEG. Other EEG findings include a diffusely slow background, runs of polyspikes during sleep, fronto-central maximum of the spikes, and periods of burst suppression. Fast spike-waves in the range of 4-6 per second may be seen as part of the myoclonic epilepsy syndromes. Spike-waves can also emerge during the evolution of a clinical tonic-clonic seizure. This does not imply that the seizure has an absence character.

Seizure Patterns

Seizures can be partial (focal) in onset or generalized in onset. Generalized seizures consist of absence, typically with 3-4 per second fronto-central generalized spike-waves; grand mal seizures with a pattern to be described below; myoclonic seizures with generalized spikes intermixed with muscle artifact; and atonic seizures with low voltage fast (electrodecremental) generalized activity. Focal seizures usually start with some local rhythm that evolves in frequency and amplitude. This rhythm may appear to be rather innocuous, such as an alpha or local theta rhythm, but the key is its evolution, and its impact on the adjacent background 238

activity. There may or may not be clinical accompaniments, such as motor activity or alterations of consciousness. If there are not, then the seizure is considered an electrographic subclinical ictal event. An intermediate stage of "subtle seizures" can develop, which really do have clinical concomitants, but only if the patient is observed carefully and tested during the electrographic episode. The above figure shows a typical focal seizure in a patient with a complex partial seizure disorder arising from the right temporal region. Rhythmical sharp activity in the 7-8 per second range begins over the right anterior temporal region, with phase reversal in the F8 electrode. Focal activity at the start of seizures can be in the theta, alpha, delta, beta range, or seizures may begin with focal spiking that builds up to a crescendo. A paradoxical response at the start of the seizure is the electrodecremental response, by which the EEG regionally or diffusely flattens. During the electrodecremental response slow activity is replaced with low voltage fast activity at the start of a seizure. This can be difficult to distinguish from a general alerting reaction, and the evolution and context provides the clue as to whether it is a seizure or not. The electroencephalographer should make careful note of the onset of the seizure to determine whether there is a focal start that then secondarily generalizes to a tonic-clonic seizure. This helps to classify the seizure as a partial onset, secondarily generalized seizure, and draws attention to the abnormal area of brain in which the seizure begins. The vast majority of studies recorded during a seizure will show abnormal EEG changes. These may represent slow waves with intermixed sharp waves, local rhythmical patterns, or regional or generalized slowing. Some changes are more specific than others, since nonfocal slowing can occur with drowsiness and hyperventilation. Rare seizures show no EEG changes on scalp electrodes. These tend to be the deep frontal seizures that do not project well to the surface. The patient may have brief and stereotyped dystonic posturing during these seizures or grimacing gestures or vocalizations, among other behaviors. Consciousness may not be lost during brief frontal seizures. Frontal lobe seizures are the most difficult type of seizure to distinguish from psychogenic seizures. Generalized seizures with loss of consciousness will always have abnormal EEG changes, with exceptions too rare to consider in an elementary exposition. The need to rule out subclinical status epilepticus is one of the indications for an emergency EEG. In this setting, a patient presents a delirium with typical waxing and waning of global cognitive functions and decreased consciousness. The question is: could this be due to seizures? EEG can be very useful in this circumstance.

EEG of Sleep
The EEG shows characteristic changes during each stage of sleep. Even the beginner needs to recognize these changes, since most EEGs include a period of sleep. Sleep is recorded because some spikes or focal slowing may only emerge during drowsiness or light sleep. The EEG is also used to assist with diagnosis of sleep disorders, but that is a specialized topic not considered here.

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A Word on Pediatric EEG

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In general, childhood EEGs show a greater degree of slowing, higher voltage, wider variability, more spikes, and a more posterior localization of natural and abnormal EEG phenomena. The reader needs to evaluate each record in light of the child's age. A perfectly normal record for a newborn would be a grossly abnormal record for an adult, and vice versa. By three years old, the EEG already has assumed most of its future adult appearance. In comparison with the adult EEG, the childs record will show more slowing, with a lot of medium or high amplitude theta activity, particularly at state changes from drowsiness to wakefulness.

Prolonged Video-EEG Monitoring

Video-EEG monitoring is useful when treatment requires clarification of the nature of the seizure or seizure-like episodes. One reason for clarification might be suspicion that the events represent one of the imitators of epilepsy, rather than epilepsy itself. Psychogenic seizures can be particularly difficult to distinguish from epileptic seizures. Another reason for video-EEG monitoring is to localize the seizure focus, prior to neurosurgery to treat intractable epilepsy. Occasionally, this monitoring may employ special invasive electrodes, such as subdural strips, grids or implanted depth wires. An increasingly attractive alternative to inpatient videoEEG monitoring is ambulatory EEG monitoring, but outpatient monitoring is not yet sufficiently reliable for presurgical localization.

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